flashcards 2

Question

What is the role of regulatory T cells (Tregs)?

Answer 1

Tregs suppress excessive immune responses and help maintain tolerance to self-antigens to prevent autoimmunity.

Answer 2

They are T cells with TCRs composed of gamma and delta chains, found mainly in mucosal tissues, and recognize lipid antigens.

Answer 3

NK cells kill virus-infected or tumor cells using receptors other than the T cell receptor.

Answer 4

ILCs help bridge innate and adaptive immunity by providing rapid defense at mucosal surfaces.

Answer 5

NKT cells express a T cell receptor (TCR) and CD3 but lack CD4 and CD8, exhibiting properties of both NK and T cells.

Answer 6

By their size, granularity, and the expression of specific surface markers (e.g., CD markers), often via flow cytometry.

Answer 7

They direct the differentiation of pluripotent stem cells into specific immune cell types by signaling through various pathways.

Answer 8

It activates T cells by displaying processed antigens on MHC molecules, thereby linking innate and adaptive immunity.

Answer 9

Innate cells provide immediate defense and antigen presentation, while adaptive cells offer specificity, memory, and regulation to effectively eliminate pathogens.

Answer 10

In 1982, scientists met in Paris to standardize the naming of immune cells by establishing the Cluster of Differentiation (CD) system, which is still in use today.

Answer 11

Granulocytes account for 60–70% of white blood cells, and about 90% of these granulocytes are neutrophils.

Answer 12

Macrophages adopt different names and characteristics depending on their tissue location—for example, Kupffer cells in the liver, alveolar macrophages in the lung, microglial cells in the brain, and histiocytes in connective tissue.

Answer 13

TCRs recognize short peptide antigens presented by MHC molecules, whereas BCRs bind directly to native antigens (usually larger proteins) and are part of the antibody production process.

Answer 14

Cytokines, interleukins, and colony stimulating factors guide the differentiation of pluripotent stem cells into specific immune cell types by signaling through various developmental pathways in the bone marrow and tissues.

Answer 15

Monocytes and macrophages are typically identified using markers such as CD14 and CD15.

Answer 16

B cells are divided into subgroups like B1 and B2, and they express surface markers such as CD19 and CD20; upon activation, they differentiate into plasma cells for antibody production or become memory cells.

Answer 17

Memory cells, derived from both T and B cells, enable a faster and more effective response when the same pathogen is encountered again.

Answer 18

Helper T cells can be subdivided into TH1 (promote cell-mediated immunity), TH2 (support humoral immunity), TH17 (involved in inflammatory responses), and TReg (regulatory) cells, each secreting distinct cytokines to modulate the immune response.

Answer 19

Primary, secondary, and tertiary lymphoid tissues.

Answer 20

They are responsible for the development, differentiation, and 'education' of lymphocytes.

Answer 21

The thymus (for T cell development) and bone marrow (for B cell development).

Answer 22

They allow the accumulation of antigen, its presentation, and interactions with naïve and memory lymphocytes to initiate immune responses.

Answer 23

Lymph nodes, spleen, and mucosa-associated lymphoid tissue (MALT).

Answer 24

They are scattered aggregations of lymphoid cells in tissues, often formed during chronic inflammation, and contain memory lymphocytes.

Answer 25

It provides an environment for T cell maturation and education.

Answer 26

It gradually shrinks (involution), becoming less functional in adulthood.

Answer 27

The outer cortex and the inner medulla.

Answer 28

Thymocytes enter as double-negative (no CD4/CD8), become double-positive (expressing both), and then are selected to become either CD4+ helper or CD8+ cytotoxic T cells.

Answer 29

Thymocytes that can bind to MHC molecules survive, ensuring they can interact with antigen-presenting cells.

Answer 30

Thymocytes that bind too strongly to self-peptides are eliminated by apoptosis to prevent autoimmunity.

Answer 31

Only about 2% of thymocytes successfully mature into naïve T cells.

Answer 32

Approximately 1–3 weeks.

Answer 33

In the bone marrow.

Answer 34

B cells that bind self-molecules too strongly undergo apoptosis to avoid autoimmunity.

Answer 35

B cells must receive survival signals in the bone marrow to mature properly.

Answer 36

It is a network of vessels that transports lymph—a fluid containing lymphocytes—between tissues, lymphoid organs, and the bloodstream.

Answer 37

They drain extracellular fluid, transport immune cells, and facilitate antigen presentation in lymphoid tissues.

Answer 38

By binding to adhesion molecules, such as LFA-1 on lymphocytes interacting with ICAM-1 on endothelial cells.

Answer 39

It is the directed migration of lymphocytes to specific tissues, guided by adhesion molecules and chemokines.

Answer 40

They are small, bean-shaped organs located at lymphatic junctions that filter antigens and facilitate immune activation.

Answer 41

The cortex (B cell follicles), the paracortex (T cells and antigen-presenting cells), and the medulla (plasma cells secreting antibodies).

Answer 42

Primary follicles are dense clusters of naïve B cells, while secondary follicles contain germinal centers where B cells proliferate after antigen exposure.

Answer 43

They enter via afferent lymphatics and exit via efferent lymphatics that drain into the bloodstream.

Answer 44

HEVs are specialized blood vessels that enable lymphocytes to enter lymph nodes from the bloodstream.

Answer 45

It filters damaged red blood cells and supports immune responses by housing lymphocytes.

Answer 46

The red pulp (which filters aged or damaged red cells) and the white pulp (which contains lymphocytes for immune responses).

Answer 47

A T cell–rich region in the spleen that surrounds arterial branches.

Answer 48

Mucosa-associated lymphoid tissue is diffuse lymphoid tissue found in the mucosal linings of the gut, respiratory, and urogenital tracts.

Answer 49

Gut-associated lymphoid tissue (GALT) and bronchus-associated lymphoid tissue (BALT).

Answer 50

They contain B cell follicles, T cells, and specialized M cells that transport antigens from the gut lumen.

Answer 51

Through M cells, which selectively transport antigens from the gut lumen to immune cells.

Answer 52

MALT lacks afferent lymphatics and directly samples antigens from mucosal surfaces.

Answer 53

Arterial pressure, smooth muscle contractions in lymphatic vessels, and backflow prevention valves maintain directional lymph flow.

Answer 54

They express homing receptors that guide their movement toward chemokine gradients.

Answer 55

They express homing receptors that bind to adhesion molecules on endothelial cells, directing them to specific tissues.

Answer 56

It is the process by which lymphocytes target the intestine by expressing receptors that bind to gut-specific endothelial molecules.

Answer 57

They continuously migrate between the blood, lymph nodes, and other secondary lymphoid tissues via the lymphatic system.

Answer 58

They are loosely organized aggregates of lymphoid cells that form at sites of chronic inflammation and may contain memory lymphocytes.

Answer 59

Each lobule of the thymus has an outer cortex and an inner medulla where thymocyte maturation occurs.

Answer 60

They assist in the development and maturation of thymocytes within the thymic cortex.

Answer 61

It undergoes apoptosis and is eliminated.

Answer 62

It undergoes negative selection (apoptosis) to prevent potential autoimmunity.

Answer 63

They undergo both positive selection, responding to survival signals, and negative selection to avoid self-reactivity.

Answer 64

Dendritic cells and macrophages process and present antigens to T cells, triggering adaptive immune responses.

Answer 65

It is the non-specific arm of the immune system that acts as the first line of defense, ready from birth.

Answer 66

Tissue damage from trauma or infection triggers the response.

Answer 67

To limit the spread of damage, eliminate microorganisms, and repair tissue damage.

Answer 68

It is active from the moment of infection (zero hours) up to about 96 hours.

Answer 69

If the pathogen is not controlled within 96 hours, adaptive immunity is recruited.

Answer 70

Phagocytes (neutrophils, monocytes/macrophages, dendritic cells), natural killer (NK) cells, innate lymphoid cells, NKT cells, gamma delta T cells, eosinophils, and B1 cells.

Answer 71

Anatomical, physiological/chemical, phagocytic/endocytic, and inflammatory barriers.

Answer 72

Physical structures like the skin and mucosal surfaces that prevent pathogen entry.

Answer 73

Its multiple layers (stratum corneum, granular, spinous, basal) and constant shedding of dead cells block microbial entry.

Answer 74

They secrete bacteriocins and metabolites (e.g., lactic acid) that inhibit pathogen growth.

Answer 75

Mucus, cilia, and secretions (urine, saliva, tears, milk) help clear and prevent microbial invasion.

Answer 76

Factors such as normal body temperature, low pH, and antimicrobial proteins/peptides.

Answer 77

It raises body temperature to inhibit pathogen growth and disrupt their metabolism.

Answer 78

The acidic conditions of the skin and stomach retard the growth of many microbes.

Answer 79

Lysozyme and lactoferrin.

Answer 80

It cleaves peptidoglycans in bacterial cell walls, particularly effective against gram-positive bacteria.

Answer 81

It sequesters essential nutrients like iron, inhibiting bacterial and fungal growth, and activates macrophages.

Answer 82

Small, cationic peptides (e.g., defensins, cathelicidins) that disrupt microbial membranes.

Answer 83

Found mainly in the respiratory tract, they bind bacterial surfaces and help clear pathogens while lubricating tissues.

Answer 84

A non-specific process where cells “drink” extracellular fluid through invagination of the plasma membrane.

Answer 85

A specific uptake process where receptors cluster in clathrin-coated pits to internalize targeted molecules.

Answer 86

A process by which specialized cells engulf and digest large particulate matter, such as pathogens.

Answer 87

Neutrophils and macrophages are the main phagocytes, with dendritic cells also contributing.

Answer 88

Recognition, ingestion, digestion, and exocytosis (which may include antigen presentation).

Answer 89

Via pattern recognition receptors (PRRs) that bind to pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs).

Answer 90

It occurs when opsonins, such as antibodies or complement proteins, coat the pathogen for enhanced uptake.

Answer 91

Molecules (e.g., antibodies, complement proteins) that coat pathogens to facilitate recognition and phagocytosis.

Answer 92

A family of pattern recognition receptors that detect PAMPs and initiate inflammatory signaling pathways.

Answer 93

TLR4 recognizes lipopolysaccharide from gram-negative bacteria.

Answer 94

TLRs activate adaptor molecules (e.g., MyD88), triggering NF-κB and MAP kinase pathways that induce inflammatory mediators.

Answer 95

They detect viral or bacterial nucleic acids (e.g., dsRNA, CpG DNA) and induce type I interferons and other cytokines.

Answer 96

C-type lectin receptors (e.g., mannose receptor, dectin-1) and scavenger receptors.

Answer 97

It binds sugars such as mannose and fucose on pathogens, aiding in recognition and phagocytosis.

Answer 98

They bind the Fc portion of antibodies that coat pathogens, enhancing opsonization and uptake by phagocytes.

Answer 99

They recognize complement proteins (e.g., C3b) deposited on pathogens, promoting phagocytosis.

Answer 100

It opsonizes pathogens, forms the membrane attack complex to lyse cells, and recruits immune cells via chemotactic signals.

Answer 101

CRP is an acute-phase protein that binds pathogens and activates the classical complement pathway.

Answer 102

They bind to and disrupt bacterial membranes by forming pores, leading to cell death.

Answer 103

Cathelicidins disrupt microbial membranes, particularly on mucosal surfaces, aiding in pathogen clearance.

Answer 104

Molecules released from damaged or dying cells that signal tissue injury and trigger inflammation.

Answer 105

They recognize conserved molecular structures (PAMPs) that are absent in host cells, while DAMPs indicate cell damage.

Answer 106

The gathering of receptors at the cell surface to form a phagocytic cup, facilitating efficient pathogen uptake.

Answer 107

Endocytosis (including pinocytosis and receptor-mediated) is for smaller particles or fluid uptake, while phagocytosis is for large particulate matter.

Answer 108

It allows antigen-presenting cells (like dendritic cells) to process pathogens and display fragments on MHC molecules to activate T cells.

Answer 109

Innate responses activate and shape adaptive immunity through antigen presentation and cytokine release.

Answer 110

NF-κB is a transcription factor that, once activated, induces the production of inflammatory cytokines and mediators.

Answer 111

MAP kinases relay signals from activated receptors to the nucleus, promoting the transcription of inflammatory genes.

Answer 112

They disrupt microbial membranes, sequester nutrients, and activate immune cells—often acting synergistically (e.g., lysozyme with lactoferrin).

Answer 113

It allows cells to specifically internalize pathogens or antigens for enhanced processing and presentation.

Answer 114

Its components (physical barriers, phagocytes, PRRs) are constitutively expressed and require no prior exposure to function.

Answer 115

They recruit immune cells, increase vascular permeability, and produce cytokines/chemokines that coordinate pathogen elimination and tissue repair.

Answer 116

NK cells are cytotoxic lymphocytes that kill virus-infected and tumor cells without prior sensitization.

Answer 117

ILCs are a diverse group that includes cells with helper functions, contributing to tissue homeostasis and inflammation.

Answer 118

NKT cells express T cell receptors yet recognize lipid antigens presented by CD1d, rapidly producing cytokines that influence both innate and adaptive responses.

Answer 119

IRFs are transcription factors activated (via TLR signaling) that induce type I interferon production, essential for antiviral responses.

Answer 120

MyD88 is the primary adaptor protein that transmits signals from most TLRs to activate downstream inflammatory pathways.

Answer 121

Clustering of receptors at the cell surface forms a phagocytic cup, enhancing the efficiency of pathogen internalization.

Answer 122

Complement receptors CR1, CR3, and CR4 on phagocytes recognize complement-opsonized pathogens and mediate their uptake.

Answer 123

Phagocytosis ingests large particles (>1 µm) by specialized cells, whereas pinocytosis involves non-specific uptake of extracellular fluid and solutes.

Answer 124

DAMPs are endogenous molecules released from damaged or dying cells that signal tissue injury and trigger inflammatory responses.

Answer 125

Surface PRRs (e.g., TLRs on the cell membrane) detect extracellular pathogens, while intracellular PRRs (e.g., RIG-I-like and NOD-like receptors) detect pathogens that invade the cytoplasm.

Answer 126

Cytokines recruit and activate immune cells, induce fever, and help amplify and direct the inflammatory response.

Answer 127

It selectively internalizes antigens via specific receptors, allowing cells to process these antigens and present fragments on MHC molecules to T cells.

Answer 128

Receptor clustering triggers the formation of pseudopodia that surround and engulf the pathogen, forming a membrane-bound phagosome; this process requires energy and cytoskeletal rearrangement.

Answer 129

Projections of the cell membrane that extend around a pathogen to engulf it.

Answer 130

The ER provides membranes used for forming phagosomes and pseudopodia, contributing to membrane recycling.

Answer 131

The phagosome fuses with lysosomes to form a phagolysosome, where enzymes degrade the engulfed pathogen.

Answer 132

Acidification of the phagolysosome and the action of enzymes like lysozyme, defensins, lactoferrin, cathelicidins, and S100 proteins.

Answer 133

The production of reactive oxygen intermediates (ROIs) and reactive nitrogen intermediates (RNIs) during the respiratory burst.

Answer 134

A rapid increase in oxygen consumption by activated phagocytes that generates ROIs to kill pathogens.

Answer 135

NADPH oxidase, which converts oxygen into superoxide radicals.

Answer 136

Through inducible nitric oxide synthase (iNOS) converting arginine to nitric oxide (NO), which can combine with superoxide to form peroxynitrite.

Answer 137

To release undigested debris, recycle membrane components, and present processed antigens for adaptive immune activation.

Answer 138

Digested antigen fragments are loaded onto MHC molecules for presentation to T cells, triggering the adaptive immune response.

Answer 139

Redness, swelling, heat, pain, and additionally a loss of function.

Answer 140

An early inflammatory response (0–24 hours) that increases blood flow, vascular permeability, and recruitment of leukocytes to the affected tissue.

Answer 141

Mast cells.

Answer 142

Mast cells, which release histamine to increase vascular permeability.

Answer 143

By upregulating adhesion molecules that enable rolling, firm adhesion, and transendothelial migration of leukocytes.

Answer 144

Rolling along the endothelium, firm adhesion, and transendothelial migration into the tissue.

Answer 145

Protein mediators produced by immune cells that regulate and coordinate the inflammatory response.

Answer 146

Interleukin-1 (IL-1), IL-6, and tumor necrosis factor-alpha (TNF-α).

Answer 147

Interleukin-10 (IL-10) and transforming growth factor-beta (TGF-β).

Answer 148

Small proteins that function as chemoattractants to direct leukocyte migration along a concentration gradient.

Answer 149

They are two major chemokine families distinguished by the spacing of cysteine residues, which correlates with their specific roles in attracting different cell types.

Answer 150

G protein-coupled receptors (GPCRs).

Answer 151

Eicosanoids (prostaglandins, leukotrienes, thromboxanes) are derived from arachidonic acid and regulate vascular permeability and leukocyte migration.

Answer 152

Cyclooxygenase (COX), particularly COX-2 in inflamed tissues.

Answer 153

Histamine increases vascular permeability and causes smooth muscle contraction, leading to redness and swelling.

Answer 154

Structures formed when neutrophils release chromatin and granule proteins to trap and kill pathogens extracellularly.

Answer 155

A form of programmed, inflammatory cell death initiated by inflammasome activation (e.g., NLRP3) that releases cytokines like IL-1β.

Answer 156

Interleukin-1β (IL-1β).

Answer 157

They enhance local blood flow, increase vascular permeability, recruit immune cells, and signal the hypothalamus to induce fever.

Answer 158

It opsonizes pathogens, induces chemotaxis, and forms the membrane attack complex to lyse pathogens.

Answer 159

By internalizing opsonized pathogens via specific receptors (e.g., Fc receptors, complement receptors) to facilitate efficient phagocytosis.

Answer 160

It enables the formation of pseudopodia and the engulfment of pathogens, making phagocytosis an energy-dependent process.

Answer 161

Adequate ATP is required for actin polymerization and other energy-dependent processes essential for effective phagocytosis.

Answer 162

Neutrophils produce a higher respiratory burst and abundant defensins for rapid killing, while macrophages use sustained lysosomal degradation and enzyme production.

Answer 163

They selectively internalize opsonized pathogens, process them, and present antigen fragments on MHC molecules to activate T cells.

Answer 164

It bridges innate and adaptive immunity, enabling a tailored T cell response to the ingested pathogen.

Answer 165

Direct recognition occurs when phagocytes use pattern recognition receptors (PRRs) to bind pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs); indirect recognition happens when opsonins (such as antibodies or complement proteins) coat pathogens, allowing receptors like Fc or complement receptors to mediate uptake.

Answer 166

The ER provides membranes that are used to form pseudopodia and phagosomes, and it assists in recycling membranes during endocytosis.

Answer 167

MHC class I presents peptides derived from cytosolic degradation (typical for intracellular pathogens), whereas MHC class II presents peptides from phagolysosomal digestion of ingested pathogens, linking innate and adaptive immunity.

Answer 168

Receptor clustering triggers cytoskeletal rearrangements that lead to pseudopodia formation and efficient engulfment of the pathogen.

Answer 169

Chemokines bind to G protein–coupled receptors (GPCRs) on leukocytes, activating signaling pathways that reorganize the cytoskeleton and direct cells along a concentration gradient toward the site of infection or injury.

Answer 170

By comparing phagocytosis with and without serum—or using serum deficient in specific complement components—researchers can distinguish between direct receptor-mediated uptake and opsonin-enhanced (indirect) phagocytosis.

Answer 171

Knockout studies and serum manipulation experiments show that when receptors (such as Fc or complement receptors) are absent or not clustered, the efficiency of pseudopodia formation and subsequent pathogen uptake is significantly reduced.

Answer 172

The kinin, clotting, fibrinolytic, and complement cascades.

Answer 173

Tissue injury activates Factor XII, which converts pre‑kallikrein to kallikrein; kallikrein then cleaves kininogen to form bradykinin, which increases vascular permeability, causes vasodilation, pain, and smooth muscle contraction.

Answer 174

Activation of Factor XII leads to thrombin generation, which converts fibrinogen to fibrin, forming clots. Fibrinopeptides released during clot formation increase vascular permeability and attract neutrophils.

Answer 175

It is triggered by endothelial damage, leading to plasmin production that degrades fibrin clots into chemotactic fragments and contributes to complement activation.

Answer 176

The classical pathway, lectin pathway, and alternative pathway.

Answer 177

By binding of antibodies (IgG or IgM) or CRP to a pathogen, which recruits the C1 complex that cleaves C4 and C2 to form the C3 convertase.

Answer 178

It cleaves C3 into C3a and C3b; C3b opsonizes pathogens and, together with other components, forms C5 convertase.

Answer 179

The lectin pathway is activated by mannose‑binding lectin (MBL) binding to sugars on the pathogen surface, which then recruits MASPs to cleave complement components similarly to the classical pathway.

Answer 180

It involves the spontaneous cleavage of C3 into C3a and C3b; C3b binds directly to microbial surfaces, associates with Factor B and D (stabilized by properdin) to form an alternative C3 convertase.

Answer 181

Opsonization of pathogens, generation of anaphylatoxins (C3a, C5a) that mediate inflammation and chemotaxis, and formation of the membrane attack complex (MAC) that causes cell lysis.

Answer 182

Sequential binding of complement components C5b, C6, C7, C8, and multiple C9 molecules forms the MAC, which inserts into pathogen membranes to cause lysis.

Answer 183

They act as anaphylatoxins that promote chemotaxis, activate phagocytes, and trigger the respiratory burst while increasing vascular permeability.

Answer 184

It encompasses the rapid cytotoxic responses by innate lymphoid cells—such as NK cells, NKT cells, γδ T cells, and B1 cells—that kill infected or abnormal cells without prior sensitization.

Answer 185

NK cells kill via (1) perforin/granzyme-mediated cytotoxicity, (2) Fas ligand-induced apoptosis, and (3) antibody-dependent cellular cytotoxicity (ADCC) through CD16.

Answer 186

NKT cells express T cell receptors that recognize lipid antigens presented on CD1 molecules, rapidly secreting cytokines that influence both innate and adaptive responses.

Answer 187

They are predominantly located in mucosal tissues and the skin, recognize non-peptide antigens, and can directly kill infected cells and secrete cytokines.

Answer 188

B1 cells produce natural, low-affinity IgM antibodies against common bacterial carbohydrate antigens, playing a critical role in early defense, especially in neonates.

Answer 189

They are interlinked cascades—initiated by tissue injury—that amplify inflammation, coordinate immune cell recruitment, and work together to contain pathogens and promote tissue repair.

Answer 190

Factor XII, when activated by tissue injury, initiates the kinin, clotting, and fibrinolytic cascades, linking vascular injury to inflammatory and hemostatic responses.

Answer 191

Cytokines (e.g., IL-1, TNF-α, IL-6) initiate and amplify inflammation, while chemokines guide the migration of leukocytes to sites of injury via GPCR signaling.

Answer 192

GPCRs on leukocytes bind chemokines, triggering intracellular signaling that reorganizes the cytoskeleton and directs cell migration along a concentration gradient.

Answer 193

Mast cells release histamine and other mediators that increase vascular permeability and promote leukocyte adhesion and extravasation.

Answer 194

Acute-phase proteins (such as CRP, serum amyloid A, and MBL) are produced by the liver in response to cytokines and act to opsonize pathogens and modulate the complement cascade.

Answer 195

Proteases from the kinin, clotting, and fibrinolytic systems generate active mediators (e.g., bradykinin, thrombin, plasmin) that increase vascular permeability, promote chemotaxis, and assist in clot formation and degradation.

Answer 196

Bradykinin causes vasodilation, increases vascular permeability, induces pain, and promotes smooth muscle contraction.

Answer 197

Thrombin converts fibrinogen into fibrin, forming clots and releasing fibrinopeptides that enhance vascular permeability and neutrophil chemotaxis.

Answer 198

Plasmin degrades fibrin clots into chemotactic fragments and helps clear clots, further modulating the inflammatory response and aiding complement activation.

Answer 199

They function as potent chemotactic agents, stimulate the respiratory burst in phagocytes, and trigger degranulation of mast cells.

Answer 200

Comparing phagocytosis with serum-free conditions (direct recognition) versus using normal or complement-deficient serum (indirect opsonization) reveals the contribution of opsonins.

Answer 201

Clustering of receptors facilitates the formation of pseudopodia and the engulfment of pathogens, making the process energy dependent and efficient.

Answer 202

It selectively internalizes opsonized pathogens, allowing for processing and subsequent presentation of antigen fragments on MHC molecules to T cells.

Answer 203

All three pathways lead to the activation of C3, resulting in opsonization, generation of anaphylatoxins, and formation of the membrane attack complex (MAC).

Answer 204

While essential for pathogen clearance, excessive complement activation and mediator release can lead to collateral tissue damage due to cytotoxic effects and oxidative stress.

Answer 205

NK cells use a balance of activatory and inhibitory receptors to detect cells with reduced MHC class I expression or stress-induced ligands, triggering cytotoxicity.

Answer 206

ADCC is a process where NK cells recognize antibodies bound to target cells through CD16, leading to the release of cytotoxic granules and target cell death.

Answer 207

CD1 molecules present lipid antigens to NKT cells, allowing for recognition and rapid cytokine production that bridges innate and adaptive responses.

Answer 208

It provides rapid cytotoxic responses against infected or abnormal cells, supplements phagocytosis, and supports the initiation of adaptive immune responses through cytokine secretion.

Answer 209

Early release of pro‑inflammatory cytokines (e.g., IL‑1, TNF‑α) initiates inflammation and recruits immune cells; later, anti‑inflammatory cytokines (e.g., IL‑10, TGF‑β) help resolve inflammation and promote tissue repair.

Answer 210

After phagocytosis, macrophages can store heavy metals (like iron) and other remnants, which may influence subsequent tissue responses and repair.

Answer 211

Autophagy is a cellular process that degrades and recycles intracellular components—including pathogens—thereby reducing infection and enhancing antigen presentation.

Answer 212

Peroxynitrite is generated when nitric oxide reacts with superoxide; it is a potent oxidant that damages microbial components, enhancing pathogen killing.

Answer 213

By comparing phagocytosis under serum‑free conditions versus serum with normal or deficient complement levels, researchers can assess the role of opsonins (antibodies/complement) in enhancing pathogen uptake.

Answer 214

C3a and C5a bind to specific receptors on immune cells, inducing chemotaxis and promoting the recruitment of phagocytes to infection sites.

Answer 215

An antigen is any substance that binds to specific receptors on lymphocytes, triggering a specific immune response.

Answer 216

An immunogen is an antigen that elicits an immune response; while all immunogens are antigens, not every antigen is immunogenic.

Answer 217

An epitope is the specific region or fragment of an antigen that is recognized and bound by an antigen receptor on a lymphocyte.

Answer 218

A hapten is a small molecule that can act as an epitope but, by itself, does not elicit an immune response unless attached to a larger carrier protein.

Answer 219

Antigens may be proteins, lipids, carbohydrates, or any combination of these, and they can be either foreign or altered self molecules.

Answer 220

Antigens enter through breaches in skin or mucosal membranes, direct injection (e.g., bites, needles), organ transplants, skin grafts, or via specialized M cells in mucosal surfaces.

Answer 221

Simple antigens are small, single molecules (like ovalbumin or pollen), while complex antigens consist of multiple antigenic determinants (such as bacterial cell wall components) on a larger structure.

Answer 222

Adjuvants enhance the immune response by increasing antigen persistence, effective size (for uptake by APCs), and by activating dendritic cells and macrophages to produce inflammatory cytokines.

Answer 223

B cell receptors recognize native, three-dimensional conformations of antigens that are free in solution or suspension.

Answer 224

TCRs recognize short, linear peptide fragments (typically 9–20 amino acids) that are processed and presented on MHC molecules by antigen-presenting cells.

Answer 225

It is a flexible Y-shaped molecule composed of two identical heavy chains and two identical light chains joined by disulfide bonds, with variable regions at the tips forming the antigen-binding sites.

Answer 226

CDRs are hypervariable loops in the variable regions of immunoglobulins that determine the specificity and affinity of antigen binding.

Answer 227

There are five classes: IgM, IgG, IgA, IgD, and IgE.

Answer 228

Naïve B cells predominantly express IgM (and IgD) as their B cell receptor.

Answer 229

Class-switch recombination changes the constant region of the immunoglobulin heavy chain, allowing the B cell to produce antibodies of a different class (e.g., IgG, IgA, or IgE) while retaining the same antigen specificity.

Answer 230

The BCR complex consists of the membrane-bound immunoglobulin (mIg) along with accessory molecules (Igα and Igβ, also known as CD79α and CD79β) that contain ITAMs for intracellular signaling.

Answer 231

The constant region allows the B cell to produce antibodies of a different class (e.g., IgG, IgA, or IgE) while retaining the same antigen specificity.

Answer 232

ITAMs (immunoreceptor tyrosine-based activation motifs) in the Igα and Igβ chains transmit signals into the cell upon antigen binding, leading to B cell activation and subsequent clonal expansion.

Answer 233

The secreted antibody and the B cell receptor have identical variable regions and antigen specificity; the BCR is the membrane-bound form of the antibody.

Answer 234

The constant region of the antibody, which differs among classes, mediates effector functions such as complement activation, binding to Fc receptors on cells, and determining antibody distribution.

Answer 235

Membrane-bound BCRs contain a transmembrane domain and a short cytoplasmic tail, whereas secreted antibodies lack the transmembrane domain and are released into circulation.

Answer 236

The CH domains (e.g., CH1, CH2, CH3) determine the class of the antibody and dictate its effector functions and interactions with complement and Fc receptors.

Answer 237

The two types are kappa (κ) and lambda (λ) light chains.

Answer 238

Diversity is generated through random gene rearrangement of variable (V), diversity (D), and joining (J) gene segments during B cell development.

Answer 239

Binding of antigen to the BCR triggers intracellular signaling via ITAMs, leading to B cell clonal expansion, differentiation into plasma cells, and formation of memory B cells.

Answer 240

Specificity is achieved by the unique antigen-binding sites on BCRs and TCRs, generated through gene rearrangements that produce a diverse repertoire capable of recognizing millions of different epitopes.

Answer 241

Vaccines work by introducing an antigen (often with an adjuvant) that elicits a specific immune response and generates long-lasting immunological memory without causing disease.

Answer 242

Antigens are internalized, processed into peptide fragments, and presented on MHC molecules by antigen-presenting cells for T cell recognition.

Answer 243

If the antigen is too small (a hapten), not in its native structure, or similar to self molecules, it may not be immunogenic without being attached to a carrier or without proper adjuvant support.

Answer 244

Factors include molecular size, complexity, dose, route of entry, and similarity to self-proteins.

Answer 245

Adjuvants increase antigen persistence, effective size, and activate innate immune cells, thereby promoting stronger antigen uptake and presentation.

Answer 246

An epitope, or antigenic determinant, is the specific part of an antigen that is recognized and bound by an antibody or T cell receptor.

Answer 247

A linear epitope consists of a continuous sequence of amino acids, whereas a discontinuous epitope is formed by amino acids that are separated in the primary sequence but come together in the protein’s 3D structure.

Answer 248

Affinity is the strength of the binding interaction between a single antigen-binding site of an antibody and a single epitope.

Answer 249

Avidity is the overall strength of binding between an antibody (with multiple binding sites) and an antigen with multiple epitopes; it represents the combined strength of all individual interactions.

Answer 250

IgM antibodies form pentamers, giving them ten antigen-binding sites that collectively provide high avidity, compensating for their lower individual affinity.

Answer 251

B cell receptors (BCRs) and T cell receptors (TCRs).

Answer 252

BCRs bind to native antigens in their three-dimensional conformation, while TCRs recognize processed peptide fragments presented on MHC molecules.

Answer 253

An antibody consists of two identical heavy chains and two identical light chains, with variable regions (for antigen binding) and constant regions (for effector functions) joined by disulfide bonds.

Answer 254

CDRs are hypervariable loops within the variable regions of immunoglobulin heavy and light chains that directly interact with the epitope and determine specificity.

Answer 255

The BCR is the membrane-bound form of the antibody; they share identical variable regions and antigen specificity, differing mainly by the presence (BCR) or absence (secreted antibody) of a transmembrane domain.

Answer 256

IgM, IgG, IgA, IgD, and IgE.

Answer 257

IgG, IgA, and IgE are produced after class switching, while naïve B cells primarily express IgM and IgD.

Answer 258

It comprises the membrane-bound immunoglobulin (BCR) along with the Igα and Igβ (CD79α/CD79β) heterodimers that contain ITAMs for signal transduction.

Answer 259

The BCR’s cytoplasmic tail is too short to signal; Igα and Igβ contain ITAMs that initiate intracellular signaling upon antigen binding.

Answer 260

A polyclonal response involves the activation and expansion of multiple clones of B or T cells, each recognizing different epitopes of the same antigen or different antigens on a pathogen.

Answer 261

Monoclonal antibodies are produced by a single B cell clone and recognize one specific epitope, whereas polyclonal responses involve antibodies from multiple clones recognizing various epitopes.

Answer 262

TCRs are heterodimers (usually composed of α and β chains, or less commonly γ and δ chains) with variable regions for antigen binding and constant regions; they remain membrane-bound.

Answer 263

TCRs recognize short peptide fragments (typically 9–20 amino acids) that are processed and presented by MHC molecules on antigen-presenting cells.

Answer 264

The TCR complex includes CD3 molecules (γ, δ, ε, and ζ chains) that contain ITAMs for signal transduction and co-receptors (CD4 or CD8) that stabilize interactions with MHC molecules.

Answer 265

TCRs are specific for peptide–MHC complexes and have a single antigen-binding site per TCR, whereas BCRs bind native antigen in their native conformation and typically have two binding sites per molecule.

Answer 266

T cells can only recognize antigens when they are presented on MHC molecules, ensuring that T cell responses are targeted and self-tolerance is maintained.

Answer 267

Superantigens are microbial proteins that bypass normal antigen processing by binding non-specifically to the variable region of TCRs and non-polymorphic regions of MHC class II, activating a large proportion (5–20%) of T cells.

Answer 268

αβ T cells, which are the majority in circulation, recognize peptides presented by MHC molecules, while γδ T cells are less diverse, are enriched in epithelial tissues, and can recognize non-peptide antigens (often presented by CD1 molecules).

Answer 269

Both contain variable and constant regions built from immunoglobulin folds, and both rely on gene rearrangement to generate diversity in their antigen-binding sites.

Answer 270

Paratopes are the antigen-binding sites on antibodies or T cell receptors, composed of the variable regions that interact with the epitope.

Answer 271

Their unique variable regions, generated by gene rearrangement, allow each lymphocyte to recognize a specific epitope, enabling a highly targeted immune response.

Answer 272

Factors include molecular size, complexity, dose, route of entry, and similarity to self-antigens.

Answer 273

Adjuvants increase antigen persistence, effective size (for uptake by APCs), and stimulate innate immune responses, thereby promoting stronger adaptive responses.

Answer 274

Affinity maturation is the process by which B cells undergo somatic hypermutation in germinal centers to increase the binding strength (affinity) of their antibodies for the antigen.

Answer 275

The variable regions are generated by random gene rearrangements and somatic mutations, allowing the immune system to produce a vast repertoire of antibodies with diverse specificities.

Answer 276

Constant regions determine the class of the antibody and mediate effector functions such as complement activation and binding to Fc receptors on immune cells.

Answer 277

It is the process by which activated B cells change the constant region of their immunoglobulin heavy chain, resulting in the production of different antibody isotypes (e.g., switching from IgM to IgG) while retaining antigen specificity.

Answer 278

T cell activation requires the binding of the TCR to a peptide–MHC complex, stabilization by co-receptors (CD4 or CD8), and signal transduction via the CD3 complex and associated kinases.

Answer 279

The immunological synapse is the interface between a T cell and an antigen-presenting cell where TCR, co-receptors, and adhesion molecules organize to facilitate effective signaling and activation.

Answer 280

A polyclonal response involves multiple B and T cell clones recognizing various epitopes of a pathogen, providing a broad and robust defense against complex antigens.

Answer 281

They are derived from a single B cell clone and recognize one specific epitope, offering consistent specificity and high affinity for diagnostic or therapeutic purposes.

Answer 282

After clonal expansion, a small population of activated lymphocytes differentiates into long-lived memory cells that enable a faster, more robust response upon re-exposure to the same antigen.

Answer 283

Antigen-presenting cells internalize antigens, process them into peptide fragments, and present these fragments on MHC molecules, which are then recognized by TCRs.

Answer 284

Co-receptors bind to conserved regions of MHC molecules, stabilizing the TCR–peptide–MHC interaction and enhancing signal transduction.

Answer 285

These interactions confer specificity to the adaptive immune response, ensuring that B and T cells precisely recognize and eliminate pathogens while also generating immunological memory.

Answer 286

Superantigens are microbial proteins that bind non-specifically to conserved regions of TCRs and MHC class II molecules, bypassing normal antigen processing and activating up to 5–20% of T cells, which can lead to an overwhelming cytokine release (cytokine storm).

Answer 287

T cells undergo positive and negative selection in the thymus; those that bind self-peptides too strongly are eliminated (negative selection), while only cells that can interact with MHC survive (positive selection), ensuring self-tolerance.

Answer 288

The CD3 complex contains ITAMs (immunoreceptor tyrosine-based activation motifs) that, upon TCR engagement, become phosphorylated to initiate intracellular signaling cascades necessary for T cell activation.

Answer 289

Activation-induced cytidine deaminase (AID) initiates class-switch recombination by deaminating cytosine bases in switch regions, allowing B cells to recombine different constant region exons and change antibody isotype without altering antigen specificity.

Answer 290

A polyclonal response involves multiple B and T cell clones recognizing different epitopes on a pathogen, ensuring a broad, robust, and effective immune defense against complex antigens.

Answer 291

MHC class I and MHC class II.

Answer 292

It consists of a single α-chain with three domains (α1, α2, α3) that form a peptide-binding groove, and is non-covalently associated with β₂-microglobulin.

Answer 293

They are expressed on all nucleated cells (and platelets).

Answer 294

β₂-microglobulin stabilizes the MHC class I α-chain and is essential for proper folding and surface expression of the molecule.

Answer 295

MHC class I presents endogenous peptides, typically 8–10 amino acids long, derived from intracellular proteins (e.g., viral proteins or mutated self-proteins).

Answer 296

Intracellular proteins are ubiquitinated and degraded by the proteasome into peptides, which are then translocated into the endoplasmic reticulum (ER) by TAP, loaded onto MHC class I molecules, and transported to the cell surface.

Answer 297

It degrades ubiquitinated proteins into peptide fragments suitable for loading onto MHC class I molecules.

Answer 298

TAP (Transporter associated with Antigen Processing) translocates peptides from the cytosol into the ER, where they can be loaded onto MHC class I molecules.

Answer 299

They are maintained in a peptide-receptive state by chaperone proteins (e.g., calnexin, calreticulin) and the peptide-loading complex (including tapasin).

Answer 300

MHC class II is composed of two polypeptide chains (α and β), each contributing two domains, forming a peptide-binding groove; both chains are transmembrane proteins.

Answer 301

Professional antigen-presenting cells (APCs) such as dendritic cells, macrophages, and B cells.

Answer 302

The invariant chain binds to the MHC class II peptide-binding groove in the ER, preventing premature peptide binding and directing the complex to the MIIC (MHC class II–enriched compartment).

Answer 303

CLIP (Class II-associated Invariant chain Peptide) is the fragment of the invariant chain that remains in the peptide-binding groove until it is replaced by an antigenic peptide.

Answer 304

HLA-DM facilitates the removal of CLIP and the binding of antigenic peptides to MHC class II molecules.

Answer 305

Peptides presented by MHC class II are usually 13–18 amino acids long.

Answer 306

MHC class I binds shorter peptides (8–10 aa) from intracellular proteins, while MHC class II binds longer peptides (13–18 aa) derived from extracellular antigens processed in endosomes.

Answer 307

MHC class I presents endogenous peptides to CD8⁺ cytotoxic T cells, whereas MHC class II presents exogenous peptides to CD4⁺ helper T cells.

Answer 308

To display peptide fragments on the cell surface in the context of MHC molecules so that T cells can recognize and initiate a specific adaptive immune response.

Answer 309

The endogenous pathway for MHC class I and the exogenous pathway for MHC class II.

Answer 310

The HLA complex (Human Leukocyte Antigen) is a set of genes on chromosome 6 that encode MHC class I and II molecules, along with other immune-related proteins.

Answer 311

HLA-A, HLA-B, and HLA-C encode MHC class I molecules.

Answer 312

HLA-DP, HLA-DQ, and HLA-DR encode MHC class II molecules.

Answer 313

They exist in many different allelic forms, especially in the peptide-binding regions, allowing a diverse range of peptides to be presented within a population.

Answer 314

Both alleles inherited from each parent are expressed, increasing the diversity of antigen presentation in an individual.

Answer 315

It increases the likelihood that some individuals can present and respond to emerging pathogens, providing resilience against infections on a population level.

Answer 316

The endogenous pathway (MHC I) processes intracellular proteins via the proteasome, while the exogenous pathway (MHC II) processes extracellular antigens in endocytic compartments.

Answer 317

Dendritic cells capture antigens in peripheral tissues, process them, and migrate to lymph nodes where they present peptide–MHC complexes to T cells.

Answer 318

Peptide binding stabilizes MHC molecules, preventing their rapid recycling and ensuring they remain on the cell surface for T cell surveillance.

Answer 319

Without bound peptides, MHC molecules are unstable and are rapidly internalized and degraded.

Answer 320

It is the structured interface between a T cell and an antigen-presenting cell where TCR, co-receptors, and adhesion molecules aggregate to facilitate effective T cell activation.

Answer 321

MHC class I presents peptides derived from intracellular (endogenous) proteins, while MHC class II presents peptides from extracellular (exogenous) proteins.

Answer 322

MHC class I, with a closed-ended peptide-binding groove, binds short peptides (8–10 aa); MHC class II, with an open-ended groove, accommodates longer peptides (13–18 aa).

Answer 323

It allows APCs to display processed peptides to T cells, thus linking the detection of pathogens (innate immunity) with the activation of antigen-specific T cells (adaptive immunity).

Answer 324

TAP transports peptides from the cytosol into the ER where they are loaded onto MHC class I molecules.

Answer 325

It is a group of chaperone proteins (e.g., tapasin, calreticulin, ERp57) that assist in peptide binding to MHC class I molecules, ensuring proper assembly and stability.

Answer 326

Antigens are internalized via endocytosis or phagocytosis, degraded in endosomes/lysosomes, and loaded onto MHC class II molecules within specialized compartments (MIIC).

Answer 327

Ii binds to the MHC class II peptide-binding groove in the ER to block premature peptide binding and directs the MHC class II molecule to endosomal compartments.

Answer 328

HLA-DM promotes the release of CLIP (the remnant of Ii) from the MHC class II groove and stabilizes the binding of antigenic peptides.

Answer 329

Because MHC molecules are highly polymorphic and co-dominantly expressed, mismatched MHC between donor and recipient can trigger strong immune rejection responses.

Answer 330

V(D)J recombination randomly rearranges gene segments in B and T cell receptors, generating a vast repertoire of receptors that can recognize millions of different antigens.

Answer 331

Over 15,000 alleles have been identified, greatly enhancing the diversity of peptide presentation in the human population and increasing resilience to pathogens while complicating organ transplantation.

Answer 332

ERAP (Endoplasmic Reticulum Aminopeptidase) trims peptide fragments to the optimal 8–10 amino acids required for stable binding to MHC class I molecules.

Answer 333

Cross-presentation is a process where certain dendritic cells present exogenous antigens on MHC class I molecules, thereby activating CD8⁺ cytotoxic T cells.

Answer 334

Professional APCs are cells specialized in processing and presenting antigens via MHC class II; they include dendritic cells, macrophages, and B cells.

Answer 335

They capture antigens in peripheral tissues, process them, and migrate to lymph nodes where they present peptide–MHC complexes to T cells, initiating the adaptive response.

Answer 336

The groove’s structure determines the peptide length and specificity—MHC class I has a closed groove (binding 8–10 aa peptides), while MHC class II has an open groove (binding 13–18 aa peptides).

Answer 337

Peptide binding stabilizes MHC molecules; empty MHC molecules are unstable and quickly recycled, reducing the efficiency of antigen presentation.

Answer 338

The endogenous pathway (MHC class I) processes intracellular proteins via the proteasome and TAP, while the exogenous pathway (MHC class II) involves uptake, degradation in endosomes, and peptide loading in MIIC compartments.

Answer 339

The invariant chain blocks the peptide-binding groove in the ER to prevent premature peptide binding and directs the MHC class II molecule to endosomal compartments for peptide loading.

Answer 340

HLA-DM facilitates the release of CLIP and the binding of antigenic peptides, while HLA-DO modulates HLA-DM activity, fine-tuning the peptide repertoire loaded onto MHC class II.

Answer 341

It ensures that both parental alleles are expressed, maximizing the variety of peptides that can be presented and enhancing immune system diversity.

Answer 342

Stable MHC-peptide complexes persist on the cell surface, increasing the chances that circulating T cells will encounter and recognize them, which is essential for effective immune monitoring.

Answer 343

It is critical for activating T cells, shaping the specificity of the immune response, and ensuring long-lasting immunological memory against pathogens.

Answer 344

An immune response that becomes more powerful following repeated encounters with the same antigen, using highly specific antigen receptors to recognise diverse pathogens and build immunological memory.

Answer 345

1) Highly diverse cell populations, 2) Pathogen-specific clonal expansion, 3) Resolution (contraction) and memory formation.

Answer 346

Naturally, via infection (e.g., chickenpox) or artificially, via vaccination (e.g., MMR, COVID).

Answer 347

To clear intracellular microbes in infected cells (CMI) and to help B cells produce varied Ig isotypes and high-affinity antibodies.

Answer 348

In the thymus, using positive selection for MHC recognition and negative selection to delete self-reactive cells (central tolerance).

Answer 349

* Naïve: Never stimulated since thymic maturation. * Effector: Short-lived, activated, perform specialised functions (cytokine secretion, cytolysis). * Memory: Long-lived, resting state after activation, rapidly reactivated on re-exposure.

Answer 350

* Naïve: Circulate through blood and lymph nodes. * Effector: Migrate to peripheral infected tissues. * Memory: Heterogeneous—some recirculate lymphoid organs, others reside in tissues.

Answer 351

Time from antigen encounter until clonal expansion (about days 0–7), before effector functions peak.

Answer 352

1. Signal 1: TCR recognition of peptide-MHC. 2. Signal 2: Co-stimulation via CD28 on T cells binding CD80/CD86 on APCs.

Answer 353

Ensures T cells activate only when APCs present antigen in an inflammatory/danger context, preventing responses to harmless or self-antigens.

Answer 354

APCs express CD80/CD86 (B7-1/B7-2 in mice), which bind CD28 on T cells.

Answer 355

Lck (lymphocyte-specific tyrosine kinase) phosphorylates ITAMs on the CD3 complex, leading to activation of transcription factors.

Answer 356

IL-2, produced after co-stimulation, drives autocrine clonal expansion (proliferation) of activated T cells.

Answer 357

It becomes anergic (non-responsive) or undergoes apoptosis, enforcing peripheral tolerance.

Answer 358

Regulatory T cells express CTLA-4, which binds CD80/CD86 more strongly than CD28, blocking co-stimulation and inducing anergy in other T cells.

Answer 359

Checkpoint inhibitors (anti-CTLA-4, anti-PD-1) unleash anti-tumour T cell responses; Nobel Prize 2018.

Answer 360

Cytokines from the same APC (and environment) that polarise activated T cells into functional subsets.

Answer 361

Th1, Th2, Th17, Treg, Tfh.

Answer 362

IL-12 (and IFN-γ/IL-18).

Answer 363

T-bet; Th1 cells produce IFN-γ, TNF-α, IL-2.

Answer 364

Activate macrophages and cytotoxic T cells for intracellular pathogen clearance (CMI).

Answer 365

GATA-3; Th2 cells produce IL-4, IL-5, IL-13.

Answer 366

Drive humoral responses against helminths and toxins; promote B cell class switching and eosinophil/mast cell activation.

Answer 367

TGF-β, IL-1, IL-6.

Answer 368

Produce IL-17, IL-22; important for mucosal barrier defence and extracellular bacterial/fungal inflammation.

Answer 369

TGF-β, IL-2.

Answer 370

Produce IL-10, TGF-β to suppress/regulate immune responses and maintain self-tolerance.

Answer 371

IL-6, IL-21.

Answer 372

Provide help to B cells in germinal centres, promoting affinity maturation and class switching (produce IL-4, IL-21).

Answer 373

IFN-γ/T-bet from Th1 inhibits GATA-3/IL-4 of Th2; IL-4/GATA-3 from Th2 inhibits T-bet/IFN-γ of Th1.

Answer 374

More co-stimulation from CD4⁺ Th cells—IL-2 production and CD40L–CD40 interactions to boost APC co-stimulation.

Answer 375

Exogenous antigens are presented on MHC I by APCs, enabling CD8⁺ T cell activation by pathogens not infecting the APC itself.

Answer 376

1. TCR–peptide–MHC recognition 2. CD28–CD80/86 co-stimulation 3. APC-derived cytokines (polarisation)

Answer 377

After antigen clearance, co-stimulation wanes; ~95% of effector T cells die by apoptosis, leaving a small memory pool.

Answer 378

Primary response shows lag then peak around day 10; secondary response is faster/higher magnitude with minimal symptoms, lasting years.

Answer 379

1) Rolling via selectins, 2) Activation by chemokines, 3) Firm adhesion via integrins, 4) Diapedesis across endothelium.

Answer 380

E-selectin and P-selectin on inflamed endothelium binding their ligands on T cells.

Answer 381

Infected tissues secrete chemokines (e.g., CXCL10), creating a gradient that activates integrins and directs T cell migration.

Answer 382

The APC’s cytokine and co-stimulatory context during activation induces specific adhesion molecules and chemokine receptors on the T cell.

Answer 383

Killing is MHC I–restricted and antigen-specific; the CTL must form a tight immunological synapse with the infected cell.

Answer 384

1) Perforin/granzyme–mediated apoptosis 2) Fas–FasL–induced caspase activation.

Answer 385

Apoptosis contains intracellular pathogens and prevents inflammation, avoiding collateral tissue damage.

Answer 386

They often use γδ or invariant αβ TCRs, recognise non-peptide antigens (lipids, metabolites), and reside in tissues (e.g., MAIT, iNKT).

Answer 387

Rapid cytokine release (IFN γ, IL-17) and cytotoxicity against stressed or infected cells, maintaining barrier immunity.

Answer 388

Via CD1d-presented glycolipids, enabling early cytokine release (e.g., IL-4, IFN γ) in mucosal tissues.

Answer 389

MR1-presented microbial vitamin B₂ metabolites at mucosal surfaces, leading to IL-17/IFN γ production.

Answer 390

Approximately 5% persist as long-lived memory T cells; ~95% die by apoptosis during contraction.

Answer 391

Loss of co-stimulation, upregulation of inhibitory receptors on T cells, and tissue wound-healing signals inducing apoptosis.

Answer 392

They enable faster, larger secondary responses upon re-encounter with the same antigen, often preventing symptomatic reinfection.

Answer 393

* Cortex: Immature thymocytes undergo positive selection on cortical epithelial cells presenting self-MHC. * Corticomedullary junction: Intermediate thymocytes receive further signals. * Medulla: Negative selection by medullary epithelial cells and dendritic cells deletes high-affinity self-reactive T cells (central tolerance).

Answer 394

* Double-negative (DN): CD4⁻CD8⁻ early precursors (DN1–4 stages) rearrange TCRβ. * Double-positive (DP): CD4⁺CD8⁺ cells express pre-TCR then rearrange TCRα before selection.

Answer 395

* Naïve T cells: Express IL-2Rβγ (intermediate affinity). * Activated T cells: Upregulate CD25 (IL-2Rα) to form the high-affinity IL-2Rαβγ complex, driving robust proliferation.

Answer 396

1. Calcineurin–NFAT (cytosolic calcium increase → NFAT activation) 2. Ras–MAPK (via LAT/Slack → AP-1 activation) 3. PKCθ–IKK (activates NF-κB).

Answer 397

* Selectins: L-selectin (naïve homing to LN), E/P-selectin ligands (inflamed tissues) * Integrins: LFA-1 (CD11a/CD18) binds ICAM-1; VLA-4 (α4β1) binds VCAM-1 for firm adhesion.

Answer 398

Activated T cells shed L-selectin, reducing lymph node recirculation and promoting migration to peripheral tissues.

Answer 399

* T_CM: CCR7⁺, CD62L⁺, home to lymphoid organs, proliferate vigorously upon re-challenge. * T_EM: CCR7⁻, CD62L⁻, patrol peripheral tissues, rapidly exert effector functions.

Answer 400

Long-lived, non-circulating cells in peripheral tissues expressing CD69 and/or CD103, providing frontline defense at barrier sites.

Answer 401

Gut dendritic cells produce retinoic acid, inducing α4β7 integrin and CCR9 on T cells for intestinal trafficking.

Answer 402

From oxidative phosphorylation in naïve cells to aerobic glycolysis (Warburg effect) in effectors, supporting biomass and rapid proliferation.

Answer 403

PD-1, CTLA-4, LAG-3 and TIM-3 upregulation dampens continued activation and promotes apoptosis of excess effectors.

Answer 404

Homeostatic cytokines IL-7 and IL-15 support memory T-cell maintenance and low-level turnover in absence of antigen.

Answer 405

Binds CD40 on APCs to upregulate CD80/86 and cytokine production, enhancing CD8⁺ T-cell priming (“licensing”) and B-cell help.

Answer 406

1) Formation of immunological synapse, 2) Polarisation of MTOC, 3) Directed release of perforin/granzymes toward target cell.

Answer 407

Inside-out signalling (via talin binding) shifts LFA-1 to a high-affinity conformation, enabling firm adhesion.

Answer 408

* Th17: TGF-β + IL-6/IL-1 → RORγt → IL-17/IL-22. * iTreg: TGF-β + low IL-6 → FoxP3 → IL-10/TGF-β.

Answer 409

T-bet suppresses GATA-3; GATA-3 suppresses T-bet; RORγt and FoxP3 reciprocally inhibit each other for Th17/Treg balance.

Answer 410

Central SMAC (TCR, CD28) and peripheral SMAC (LFA-1/ICAM) zones organising sustained signalling and adhesion.

Answer 411

Upon synapse formation, CTLs upregulate FasL on their surface, engaging Fas on target to trigger caspase-8-mediated apoptosis.

Answer 412

* Strong, sustained CD28 signalling + high IL-2: Favors effector differentiation. * Weak/brief co-stimulation: Promotes memory precursor formation and long-lived memory.

Answer 413

Generate vast lymphocyte diversity to match pathogens, expand and refine matched clones, and maintain memory for future protection.

Answer 414

BCRs are membrane-bound (or secreted as antibody), recognise intact antigen, and have class-determining Fc regions; TCRs bind peptide-MHC only on other cells.

Answer 415

Neutralisation (toxins/viruses), opsonisation (phagocytosis), complement activation, agglutination, and antibody-dependent cell-mediated cytotoxicity (ADCC).

Answer 416

RAG1 and RAG2 (Recombination Activating Genes) catalyse combinatorial joining of V, D, and J segments in the bone marrow.

Answer 417

V, D, and J gene segments (VDJ), plus the constant (C) region determining isotype.

Answer 418

V and J segments (VJ), with either kappa or lambda light chains paired with heavy chain.

Answer 419

Protein diversity = (#V)×(#D)×(#J); e.g., 6 V × 4 D × 3 J = 72 heavy-chain possibilities.

Answer 420

Addition (by TdT) or deletion of nucleotides at V–D–J junctions, boosting diversity beyond combinatorial potential.

Answer 421

On the order of 10 billion distinct specificities.

Answer 422

Somatic hypermutation and class-switch recombination, both requiring AID in the germinal centre.

Answer 423

Activation-Induced Cytidine Deaminase (AID).

Answer 424

Sequential Cμ → Cδ → Cγ3 → Cγ1 → Cα1 → Cγ2 → Cγ4 → Cε → Cα2 segments, recombined by AID to change isotype.

Answer 425

Membrane receptor on naïve B cells; no secreted effector role.

Answer 426

First isotype expressed; forms pentamers; potent complement activator; bulky, doesn’t cross placenta.

Answer 427

Four subclasses (IgG1–4) differ in hinge length and Fc-mediated functions such as opsonisation and ADCC.

Answer 428

Mucosal protection; secreted as dimer into secretions (milk, saliva); resists gut proteases.

Answer 429

Binds mast-cell FcεR in absence of antigen; crosslinking triggers degranulation; key in parasitic defense and allergy.

Answer 430

T-independent type I: polyclonal activation via pattern-recognition receptors (e.g., TLR ligands) without specific BCR engagement.

Answer 431

T-independent type II: repetitive antigen arrays (e.g., bacterial polysaccharides) crosslink many BCRs; minimal memory formation.

Answer 432

Protein antigens processed and presented on MHC II to CD4⁺ T-cells; require T-cell help for CSR, SHM, and memory formation.

Answer 433

“Signal 1”: BCR-mediated antigen uptake and presentation; “Signal 2”: CD40–CD40L interaction plus cytokines from T helper cells.

Answer 434

CD40 (on B cells) interacting with CD40L (CD154) on T fh cells promotes proliferation, survival, and CSR.

Answer 435

Dark zone: centroblasts proliferate and hypermutate; light zone: centrocytes compete for antigen on FDCs and T fh help, undergoing selection.

Answer 436

Iterative cycles: SHM in dark zone → selection of higher-affinity BCRs in light zone → re-entry or differentiation into memory/plasma cells.

Answer 437

High-affinity B cells differentiate into long-lived plasma cells (antibody secretion) or memory B cells for rapid recall.

Answer 438

Outside germinal centres early in TD responses; secrete unmutated IgM before GC formation.

Answer 439

It induces T-dependent GC responses, generating high-affinity, class-switched antibodies and durable memory B cells over time.

Answer 440

A technique that hydrodynamically focuses cells in suspension into a single‐cell stream, then measures light scattering and laser‐excited fluorescence to analyse cell properties at high throughput

Answer 441

* Forward scatter (FSC): proportional to cell size * Side scatter (SSC): proportional to internal complexity/granularity

Answer 442

A high‐velocity sheath fluid surrounds the sample stream, aligning cells into a single file so each cell passes one at a time through the laser interrogation point

Answer 443

They bind specific cell markers; when excited by lasers, each fluorophore emits light at a characteristic wavelength, enabling multiplexed detection of multiple markers on the same cell

Answer 444

The number of lasers (excitation wavelengths) and detectors (emission filters) available; modern instruments can detect 12–28 colors, with some advanced systems detecting up to ~60

Answer 445

Each fluorochrome has a unique excitation/emission spectrum; filters isolate emitted wavelengths so signals are attributed to the correct fluorochrome

Answer 446

A user‐defined region on a scatter or fluorescence plot that selects a cell subset of interest (e.g., lymphocytes by FSC/SSC) for further analysis

Answer 447

1. Gate on lymphocytes (low FSC, low SSC) 2. Stain with anti-CD3 and anti-CD4 fluorophore-conjugated antibodies 3. Gate on CD3⁺CD4⁺ double-positive cells

Answer 448

RBCs lack nuclei and burst in lysis buffer (e.g., ammonium chloride), allowing removal of debris and haemoglobin while preserving more robust leukocytes for analysis

Answer 449

Natural fluorescence emitted by cells when excited; measured using an unstained control to set fluorescence gates above background

Answer 450

A fluorophore-conjugated antibody of the same species, isotype, and concentration but against an irrelevant antigen; measures non-specific binding via Fc receptors or sticky interactions

Answer 451

* Unstained control: measures autofluorescence * Isotype control: measures non-specific binding * Test sample: contains specific fluorophore-tagged antibodies

Answer 452

* Immunophenotyping (e.g., CD4:CD8 ratio in HIV) * Live/dead assays * Cell cycle analysis * Cytokine production * Phagocytosis assays * Telomere length measurement

Answer 453

* Lymphocytes: low FSC, low SSC * Monocytes: intermediate FSC, SSC * Granulocytes: high FSC, high SSC

Answer 454

Because fluorescence signals vary over orders of magnitude; log scales spread out data to distinguish dim and bright populations

Answer 455

Mean fluorescence intensity correlates with antigen density: brighter signal indicates higher protein expression per cell

Answer 456

The percentage of events discarded when cells pass too close together; low abort rates (<1%) ensure accurate high‐throughput data (e.g., 3,000–10,000 events/sec)

Answer 457

1. Determine % events in each quadrant of gated plot 2. Sum relevant quadrants for combined subsets (e.g., CD3⁺ = CD3⁺CD4⁺ + CD3⁺CD4⁻) 3. Calculate ratios or % of parent population

Answer 458

* Larger cell size (e.g., activated T cells) * Granularity (e.g., granulocytes) * Culture conditions (e.g., media components)

Answer 459

To minimise spectral overlap, ensure each fluorochrome is excited by available lasers and detected with appropriate filters, and include necessary controls for compensation and gating

Answer 460

It provides baseline counts and proportions of red and white blood cells; deviations can indicate disease and guide which subsets to analyse by flow cytometry.

Answer 461

By hydrodynamically focusing cells in single‐file through a laser beam and measuring light scatter (size/granularity) and fluorophore‐emitted fluorescence for specific markers.

Answer 462

“Cluster of Differentiation” surface markers uniquely expressed on cell types (e.g., CD3 on T cells, CD4 on helper T cells); targeted by fluorophore‐conjugated antibodies for identification.

Answer 463

A fluorophore‐conjugated antibody of the same isotype but irrelevant specificity; measures non‐specific binding and sets accurate fluorescence gates.

Answer 464

To prevent photobleaching of fluorophores, which reduces their fluorescence intensity and accuracy of detection.

Answer 465

Proportions and absolute counts of T‐cell subsets, cell size/granularity profiles, and assessment of staining specificity via isotype controls.

Answer 466

Random V(D)J gene rearrangements create diverse TCRs/BCRs, but can produce self-reactive lymphocytes that cause autoimmunity (“horror autotoxicus”) without tolerance mechanisms

Answer 467

Deletion or editing of self-reactive T cells in the thymus and B cells in the bone marrow before they enter circulation

Answer 468

In the thymic cortex, thymocytes that bind self-MHC weakly receive survival signals; non-binders die by apoptosis

Answer 469

In the thymic medulla, medullary epithelial cells and DCs present self-antigens; thymocytes with high-affinity self-MHC binding undergo apoptosis

Answer 470

In the bone marrow, self-reactive B cells may: 1. Undergo receptor editing (light-chain recombination) 2. Die by apoptosis if editing fails 3. Become anergic if binding is weak

Answer 471

Not all self-antigens are expressed in primary lymphoid organs; deleting all self-reactive cells would overly narrow the repertoire; environmental antigens aren’t encountered centrally

Answer 472

Mechanisms acting on mature T and B cells in the periphery to control any self-reactive cells that escaped central tolerance

Answer 473

Some self-antigens are hidden (sequestered) or expressed at low levels and never reach activation threshold, so T cells remain unresponsive

Answer 474

TCR engagement without co-stimulation (CD28–CD80/86) or active inhibition by CTLA-4, leading to unresponsiveness on restimulation

Answer 475

Upregulated after T-cell activation; binds CD80/86 with higher affinity than CD28, sending inhibitory signals and suppressing APCs

Answer 476

Repeated TCR stimulation induces Fas/FasL and pro-apoptotic proteins (Bax, Bad, Bim), triggering apoptosis of self-reactive T cells in the periphery

Answer 477

* Contact-dependent: High CTLA-4 expression binds APCs, can directly kill via perforin/granzyme * Soluble factors: Secrete IL-10 and TGF-β; “mop up” IL-2 via low-affinity IL-2R

Answer 478

* Natural Tregs: Develop in the thymus, express FoxP3 intrinsically * Inducible Tregs: Arise in periphery from naïve CD4⁺ T cells upon antigen + tolerogenic signals

Answer 479

Chronic low-level antigen and BCR cross-linking without adequate co-stimulation (e.g., CD40L, TLR signals) renders B cells unresponsive

Answer 480

High-level antigen cross-linking without T-cell help triggers B-cell apoptosis via intrinsic death pathways

Answer 481

Partially activated B cells fail to express homing chemokine receptors, so cannot enter follicles or receive survival signals to mature

Answer 482

FcγRIIB engagement by immune complexes delivers inhibitory signals; limited BAFF (survival factor) can also cause B-cell death

Answer 483

Failure in central or peripheral tolerance allows self-reactive lymphocytes to persist and attack tissues, mediated by hypersensitivity II–IV mechanisms

Answer 484

Susceptibility genes (e.g., HLA-DQ/DR alleles) plus triggers (infections, hormones, gut dysbiosis) combine to breach tolerance

Answer 485

The anterior chamber of the eye or areas behind the blood–brain barrier, where antigens remain sequestered from immune surveillance

Answer 486

They contribute to tumor surveillance and help regulate normal inflammatory responses, balancing immunity with tolerance

Answer 487

An excessive or misdirected normal immune response that causes tissue damage when regulatory mechanisms fail or responses occur at the wrong time

Answer 488

By the Gell & Coombs system into four types: * Type I: IgE-mediated (immediate) * Type II: IgG/IgM-mediated (antibody against cell/tissue antigens) * Type III: Immune complex-mediated * Type IV: T cell-mediated (delayed)

Answer 489

* Antibody-mediated: Types I, II, III * Cell-mediated (delayed): Type IV

Answer 490

1. Sensitisation: First exposure → Th2-driven B cells class-switch to IgE → IgE binds FcεRI on mast cells. 2. Elicitation: Re-exposure → Allergen cross-links mast-cell IgE → Immediate degranulation and mediator release

Answer 491

* Pre-formed: Histamine, proteases * Newly synthesized: Prostaglandins, leukotrienes, cytokines (e.g., TNF)

Answer 492

IL-4 (class switching to IgE) and IL-5 (eosinophil activation)

Answer 493

Allergic rhinitis (hay fever), Asthma, Systemic anaphylaxis

Answer 494

IgG or IgM auto- or allo-antibodies bind cell-surface or matrix antigens → Fc receptor–mediated phagocytosis/ADCC and/or complement fixation → tissue injury

Answer 495

Type II: Antibody-mediated cell/tissue destruction Type V: Antibody-mediated functional modulation of receptors (e.g., Graves’ disease)

Answer 496

Autoimmune haemolytic anaemia (anti-RBC antibodies → phagocytosis/MAC), Goodpasture’s syndrome (anti-GBM IgG → glomerulonephritis)

Answer 497

Graves’ disease (anti-TSH-receptor → hyperthyroidism), Myasthenia gravis (anti-AChR → muscle weakness)

Answer 498

Normally phagocytosed by macrophages; excess small complexes deposit in vessel walls → complement activation + neutrophil recruitment → inflammation and tissue damage

Answer 499

Small complexes: Deposit in blood vessels → vasculitis Large complexes: Cleared in liver/spleen; may accumulate in kidneys if complement deficient

Answer 500

Serum sickness (e.g., anti-snake venom), Systemic lupus erythematosus (anti-DNA immune complexes → glomerulonephritis)

Answer 501

Sensitised T cells (mainly Th1) release IFN-γ on re-exposure (1–2 weeks) → macrophage activation and/or CTL-mediated cytotoxicity → tissue damage

Answer 502

A small molecule that binds host proteins → presented on MHC I/II → CD8⁺ CTLs kill cells and Th1 cells activate macrophages → rash (e.g., poison ivy)

Answer 503

Persistent antigen (e.g., Mycobacterium tuberculosis) → Th1-driven IFN-γ activates macrophages → fused “giant” cells form granuloma to contain infection

Answer 504

Tuberculosis, sarcoidosis, Crohn’s disease

Answer 505

T cell priming and recruitment of macrophages take 24–72 hours to develop inflammation upon antigen re-exposure

Answer 506

I: IgE & mast cells, immediate (<1 hr) II: IgG/IgM & complement/ADCC, hours III: Immune complexes & neutrophils, hours IV: T cells & macrophages/CTLs, delayed (1–2 days)

Answer 507

Occurs 4–12 hours after initial mast-cell degranulation; driven by newly synthesized mediators (e.g. leukotrienes, cytokines) causing sustained inflammation (e.g. bronchospasm, edema).

Answer 508

H₁‐antagonists (e.g. diphenhydramine) block histamine-mediated itch/vasodilation Leukotriene receptor antagonists (e.g. montelukast) reduce bronchoconstriction Epinephrine reverses laryngeal edema and hypotension in anaphylaxis

Answer 509

H₁ receptors on smooth muscle and endothelium.

Answer 510

A localized Type III vasculitis seen after intradermal injection of antigen in pre-immunized individuals; immune complexes form in vessel walls causing edema, hemorrhage.

Answer 511

Serum sickness is systemic—large quantities of antigen (e.g. antitoxin) generate immune complexes that deposit in vessels, joints, and kidneys days after injection.

Answer 512

Small complexes are less efficiently cleared by spleen/liver macrophages and can slip through endothelium into tissues.

Answer 513

The classical pathway, initiated by C1 binding IgG/IgM in complexes, generates C5a to recruit neutrophils.

Answer 514

IVa: Th1-macrophage (e.g. PPD test) IVb: Th2-eosinophil (e.g. chronic asthma) IVc: CTL-mediated (e.g. Stevens–Johnson syndrome) IVd: T-cell–neutrophil (e.g. acute generalized exanthematous pustulosis)

Answer 515

Intradermal PPD injection; induration measured at 48–72 h. ≥5–15 mm of firm swelling indicates prior sensitization.

Answer 516

A Type IVa reaction to haptens (e.g. nickel) on skin—erythema and vesicles develop 24–48 h after contact.

Answer 517

IFN-γ from Th1 cells, activating macrophages to wall off persistent antigens.

Answer 518

It acts as a hapten, binding RBCs—and anti‐penicillin antibodies mediate complement lysis (hemolytic anemia).

Answer 519

C1q binding or CH50 assay—low complement levels indicate ongoing consumption by complexes.

Answer 520

CD8⁺ cytotoxic T lymphocytes via perforin/granzyme (e.g. in Stevens–Johnson syndrome).

Answer 521

Immediate (Type I): Skin‐prick test read in 15–20 min for wheal‐and‐flare (IgE) Delayed (Type IV): Patch or intradermal test read at 48–72 h for induration (T cells).

Answer 522

They’re the major entry points for pathogens (gut, lung, genitourinary tracts), require discrimination between harmful microbes and harmless antigens, and host ~80% of all immune cells.

Answer 523

Mucosa-Associated Lymphoid Tissue, including GALT (gut), BALT (bronchial), and NALT (nasopharynx).

Answer 524

1) Defence against invasive pathogens, 2) Prevention of responses to commensal flora and food antigens (mucosal tolerance).

Answer 525

Blood → spleen; Skin → draining lymph nodes; Mucosa → MALT (e.g., Peyer’s patches for gut antigens).

Answer 526

Peyer’s patches, appendix, and scattered (pseudo-follicles) intraepithelial lymphocytes.

Answer 527

1) Physical barrier (mucus, epithelium), 2) Innate immunity (DCs, macrophages, ILCs), 3) Adaptive immunity (sIgA, Th17, Tregs).

Answer 528

Glycoproteins (e.g., MUC2) from goblet cells, antimicrobial peptides (e.g., defensins) from Paneth cells, plus secretory IgA.

Answer 529

They maintain selective permeability, preventing most microbes and large molecules from crossing into tissue.

Answer 530

Attracted by epithelial MIP3α, they help maintain barrier integrity and secrete cytokines upon activation.

Answer 531

They extend dendrites between enterocytes to sample lumenal antigens, produce IL-10/TGF-β (tolerogenic), and promote IgA class-switching and Treg differentiation.

Answer 532

Sustained TLR signals from invasive pathogens; they then secrete IL-1, IL-6, TNFα and recruit ILCs and Th17 cells.

Answer 533

Inductive site (antigen uptake/activation) and effector site (armed lymphocytes migrate to lamina propria).

Answer 534

M (microfold) cells, which transcytose antigen from the lumen to sub-epithelial APCs.

Answer 535

M cells → DCs capture antigen → conditioned by epithelial TGF-β → DCs induce Th2/Tregs → B cells class-switch to IgA → plasma cells migrate to lamina propria.

Answer 536

TGF-β, IL-10 and CD40L from Tfh/Tregs in germinal centres.

Answer 537

Dimeric IgA binds pIgR on basolateral surface, is transcytosed, and pIgR is cleaved to release secretory component–bound sIgA.

Answer 538

Neutralises pathogens/toxins, prevents microbial adherence, aids clearance, without fixing complement or inducing inflammation.

Answer 539

Compensation by other isotypes (e.g., IgM) and intact physical/innate barriers.

Answer 540

Epithelial TLRs → IL-1, IL-6, TNFα → DC/ILC1 activation → Th17 differentiation (with TGF-β, IL-6, IL-1) → IL-17A/IL-22 secretion → neutrophil recruitment and AMP production.

Answer 541

IL-17A (neutrophil recruitment/activation) and IL-22 (antimicrobial peptides, increased permeability).

Answer 542

Dominant Th2/ILC2 response (IL-4, IL-5, IL-13) leading to eosinophil recruitment and barrier repair.

Answer 543

High Treg/IL-10/TGF-β environment, tolerogenic DC conditioning, and sIgA–mediated exclusion.

Answer 544

Conditions DCs to a tolerogenic phenotype, promotes IgA class-switching and Treg differentiation.

Answer 545

They extend processes between tight-junctioned epithelial cells into the lumen to capture pathogens.

Answer 546

Plasma cells (sIgA), CD4⁺/CD8⁺ T cells, and innate lymphoid cells.

Answer 547

Genetic susceptibility + abnormal microbe interactions → excessive Th1/Th17 inflammation, granuloma formation, transmural lesions.

Answer 548

Crohn’s: Any GI region, transmural inflammation, granulomas UC: Colon only, mucosal layer, crypt abscesses, cancer risk.

Answer 549

Western diet, altered microbiota, vitamin D deficiency, smoking, medications.

Answer 550

HLA haplotypes and polymorphisms in epithelial/immune genes increase susceptibility; family/twin studies show heritability.

Answer 551

Epithelial cells secrete MIP3α, which recruits ILC1, ILC2, and ILC3 to maintain barrier integrity.

Answer 552

HLA haplotypes and polymorphisms in epithelial/immune genes increase susceptibility; family/twin studies show heritability

Answer 553

Epithelial cells secrete MIP3α, which recruits ILC1, ILC2, and ILC3 to maintain barrier integrity

Answer 554

ILC1: Produce IFN-γ, mirror Th1, defend against intracellular pathogens ILC2: Produce IL-5/IL-13, mirror Th2, drive anti-helminthic responses and tissue repair ILC3: Produce IL-17/IL-22, mirror Th17, promote neutrophil recruitment and antimicrobial peptide production

Answer 555

M cells express PRRs (e.g., TLRs) on their apical surface, take up lumenal antigen by transcytosis, and hand it to sub-epithelial DCs/macrophages

Answer 556

TLR-activated enterocytes release TGF-β and growth factors that “condition” DCs to a tolerogenic phenotype, promoting Treg induction and IgA switching

Answer 557

1. Dimeric IgA (with J chain) binds pIgR on basolateral epithelium 2. The complex is transcytosed 3. Proteolytic cleavage releases sIgA with its secretory component into the lumen

Answer 558

Over 75% of body immunoglobulin is IgA, with around 3 g secreted into mucosae each day

Answer 559

sIgA does not fix complement, activate granulocyte degranulation, or induce full DC maturation—its role is homeostatic exclusion and neutralisation without inflammation

Answer 560

HLA-DQ/DR haplotypes Polymorphisms in epithelial and immune genes Monozygotic twin concordance ~50% for Crohn’s, ~20% for UC

Answer 561

Western diet, altered microbiota, vitamin D deficiency, certain medications, and smoking all increase susceptibility

Answer 562

Crohn’s: Transmural lesions, granulomas, anywhere in GI (often ileum), Th1/Th17-driven, anti-bacterial IgG UC: Mucosal-only inflammation, crypt abscesses, colon-restricted, mixed Th1/Th2, increased carcinoma risk

Answer 563

Approximately 61 V, 27 D, and 6 J segments, recombined to form heavy-chain variable regions

Answer 564

Kappa: ~48 V and 5 J segments; Lambda: ~40 V and 7 J segments

Answer 565

FW1–CDR1–FW2–CDR2–FW3–CDR3: CDR3 (formed at V–(D)–J junction) is the most hypervariable for antigen binding

Answer 566

* Exonucleolytic trimming removes random nucleotides at V/D/J ends * TdT-mediated N-region addition inserts random nts at junctions

Answer 567

Estimates ~10 billion possible unique receptors

Answer 568

Activation-induced cytidine deaminase (AID) in germinal-centre B cells

Answer 569

* Extrafollicular: Rapid, short-lived IgM plasma blasts, no SHM or CSR * Germinal-centre: Slower, high-affinity, class-switched memory/plasma cells via SHM & CSR

Answer 570

* Dark zone: Centroblasts proliferate and hypermutate * Light zone: Centrocytes compete for antigen on FDCs and Tfh help, undergoing selection

Answer 571

AID excises intervening constant genes; once downstream isotypes (e.g. IgA2) are reached, upstream ones cannot be re-acquired

Answer 572

* TI-1: Polyclonal activation via TLRs (e.g. CpG), independent of BCR specificity * TI-2: Repetitive non-protein antigens (e.g. bacterial polysaccharides) crosslink many BCRs; minimal memory

Answer 573

1. Signal 1: BCR binds and processes protein antigen → pMHC II presentation 2. Signal 2: CD40L on T fh engages CD40 on B cell + cytokines

Answer 574

Display native antigen–antibody complexes for centrocyte BCR testing, guiding selection of high-affinity clones

Answer 575

* Memory B cells: Recirculate, rapidly re-enter GCs on rechallenge * Plasma cells: Migrate to bone marrow niches to continuously secrete high-affinity Ab

Answer 576

* Plasmablasts: Peak ~Day 7 after 1st dose (extrafollicular) * Memory B cells: Peak ~Day 7 after 2nd dose (GC-derived)

Answer 577

B-cell clones hypermutate randomly; only those with improved affinity capture antigen/Tfh help and survive to become memory/plasma cells

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