immunology

Question 1

What are the three lines of immune defense?

Answer 1

1) Physical/chemical barriers (e.g., skin, mucosa); 2) Innate immunity (e.g., macrophages, neutrophils); 3) Adaptive immunity (T and B cells).

Question 2

Which cells make up the innate immune system?

Answer 2

Macrophages, neutrophils (PMNs), dendritic cells, natural killer (NK) cells; they act rapidly and can travel through blood and lymph to the site of infection.

Question 3

What characterizes neutrophils (PMNs)?

Answer 3

Aggressive, short-lived, multilobed nuclei; act as APCs and activate naïve T cells.

Question 4

What is the function of NK cells?

Answer 4

They kill virally infected cells and tumor cells, particularly those with reduced MHC I expression, using perforin and granzymes.

Question 5

How do epithelial surfaces protect against pathogens?

Answer 5

They form physical barriers (e.g., skin) and secrete mucus (e.g., in airways, stomach, cervix, cornea) to trap and clear pathogens.

Question 6

What happens when keratinocytes are damaged?

Answer 6

They release pro-inflammatory cytokines like TNF and IL-8, which lead to inflammation.

Question 7

What is the role of PRRs (Pattern Recognition Receptors)?

Answer 7

PRRs detect PAMPs and activate signaling pathways (e.g., NF-kB) to trigger inflammation. Includes TLRs, NOD-like receptors, and C-type lectins.

Question 8

How are chemokines classified and what is their role?

Answer 8

Chemokines are grouped into CXC, CC, CX3C, and C subfamilies. They direct cell movement via chemotaxis, affecting leukocyte recruitment during infection.

Question 9

What is the complement system and its function?

Answer 9

A set of ~30 proteins that enhance antibody and phagocytic responses, clear microbes, promote inflammation, and directly lyse pathogens.

Question 10

What are the three complement activation pathways?

Answer 10

1) Classical (antibody-antigen complex); 2) Alternative (pathogen surfaces); 3) Lectin (mannose-binding lectin binding to microbes).

Question 11

What is opsonization?

Answer 11

Coating a pathogen with antibodies or complement proteins (e.g., C3b) to enhance phagocytosis.

Question 12

What is MHC and why is it important?

Answer 12

Major Histocompatibility Complex presents peptide antigens to T cells. MHC I presents endogenous antigens to CD8+ cells; MHC II presents exogenous antigens to CD4+ cells.

Question 13

What determines whether an organ transplant is rejected?

Answer 13

Mismatch of MHC molecules between donor and recipient triggers immune rejection.

Question 14

What are naïve vs. effector T cells?

Answer 14

Naïve: never encountered antigen. Effector: activated, proliferated, capable of killing or helping other cells.

Question 15

What is required for T cell activation?

Answer 15

1) TCR binding to MHC-peptide complex; 2) Co-stimulation via CD28-B7; 3) Adhesion via LFA1-ICAM1.

Question 16

What are the subsets of CD4+ T cells?

Answer 16

Th1 (intracellular defense), Th2 (extracellular pathogens, worms), Th17 (neutrophil activation), Treg (immune suppression), Tfh (B cell help).

Question 17

What cytokines influence CD4+ subset differentiation?

Answer 17

Th1: IL-12, IFN-γ; Th2: IL-4; Th17: IL-6, TGF-β; Treg: TGF-β; Tfh: IL-21.

Question 18

How do CD8+ cytotoxic T cells kill?

Answer 18

Release perforin (forms pores) and granzymes (enter cell to induce apoptosis); recognize antigen on MHC I.

Question 19

What is the difference between primary and secondary immune responses?

Answer 19

Primary: faster rxn but slower recovery, max ~10 days; Secondary: slower rxn faster recovery (~4 days), stronger due to memory B and T cells.

Question 20

What are B cells and what do they do?

Answer 20

Produce antibodies that neutralize pathogens and mark them for destruction. Have membrane-bound antibodies as B cell receptors (BCRs).

Question 21

How do B and T cells interact?

Answer 21

Occurs in lymph node paracortex. B cell presents antigen on MHC II to CD4+ T helper t cells cell. CD40-CD40L and antigen recognition are required for activation.

Question 22

What is class switch recombination?

Answer 22

T cell cytokines (e.g., IL-4, IFN-γ, TGF-β) guide B cells to switch antibody isotype (e.g., IgM → IgG, IgA, IgE) for better immune function.

Question 23

What are the types of B cell responses?

Answer 23

1) Thymus-dependent (requires T cell help); 2) Thymus-independent (e.g., TLR ligands or polysaccharides; leads to short-lived IgM response).

Question 24

What is immune tolerance?

Answer 24

The lack of immune response to specific antigens, especially self-antigens. Can be central (thymus/bone marrow) or peripheral (in tissues).

Question 25

What are the mechanisms of peripheral tolerance?

Answer 25

1) Deletion (apoptosis); 2) Anergy (due to lack of co-stimulation, e.g., CTLA-4); 3) Suppression (via regulatory T cells).

Question 26

What are the four types of hypersensitivity reactions?

Answer 26

Type I: IgE-mediated allergy (immediate); Type II: IgG/IgM to cell surfaces (e.g., hemolysis); Type III: Immune complexes; Type IV: T-cell mediated (delayed).

Question 27

What is anaphylaxis and how is it treated?

Answer 27

Severe systemic allergic reaction (Type I) causing airway obstruction and hypotension. Treated with epinephrine injection.

Question 28

What is central tolerance and its key feature?

Answer 28

Occurs in thymus/bone marrow. Self-reactive lymphocytes are deleted via expression of Aire gene (T cells) or rendered nonresponsive (B cells).

Question 29

What is immune privilege and where does it occur?

Answer 29

Sites like the eye, brain, and fetus are protected from immune responses, reducing inflammation in sensitive tissues.

Question 31

What role do dendritic cells (DCs) play in the immune response?

Answer 31

Immature DCs capture antigens and mature in response to cytokines and chemokines, upregulating MHC II and co-stimulatory receptors to present antigens to T cells in lymphoid tissue.

Question 32

What is the function of Langerhans cells?

Answer 32

Langerhans cells are a subset of dendritic cells found in the skin that capture and transport antigens to lymph nodes for T cell activation.

Question 33

What determines the compatibility for organ transplants?

Answer 33

The compatibility of MHC (HLA in humans) molecules; mismatched MHC leads to transplant rejection due to immune recognition of non-self.

Question 34

What is MHC restriction in T cell responses?

Answer 34

T cells only recognize antigens presented with specific MHC molecules—CD8+ T cells with MHC I and CD4+ T cells with MHC II. This determines immune specificity.

Question 35

What is the difference in peptide length between MHC I and MHC II molecules?

Answer 35

MHC I presents peptides 8–10 amino acids long; MHC II presents longer peptides, 12–18 amino acids.

Question 36

How are endogenous and exogenous antigens processed?

Answer 36

Endogenous antigens (from inside cells, e.g., viruses) are presented on MHC I; exogenous antigens (from outside, e.g., bacteria) are processed and presented on MHC II.

Question 37

What cytokine is critical for CD8+ T cell proliferation?

Answer 37

Interleukin-2 (IL-2) is crucial for the proliferation of activated CD8+ cytotoxic T lymphocytes.

Question 38

What is the role of perforins and granzymes in CD8+ T cell killing?

Answer 38

Perforins form pores in the target cell membrane. Granzymes enter through the pores to induce apoptosis by fragmenting DNA and disrupting proteins.

Question 39

What is the role of Tfh cells?

Answer 39

T follicular helper (Tfh) cells express CXCR5 and assist B cells in germinal centers to produce high-affinity, class-switched antibodies.

Question 40

What is immunological memory?

Answer 40

After antigen exposure, some T and B cells become long-lived memory cells that respond faster and stronger upon re-exposure to the same antigen.

Question 41

What are the main outcomes of CD4+ T cell activation?

Answer 41

Depending on the subset, they help activate B cells (Tfh), enhance phagocyte killing (Th1), support antibody production (Th2), promote inflammation (Th17), or suppress immunity (Treg).

Question 42

What is CTLA-4 and how does it induce T cell anergy?

Answer 42

CTLA-4 competes with CD28 for B7 binding on APCs. Its binding fails to provide co-stimulation and leads to T cell anergy, preventing activation.

Question 43

What are examples of immunologically privileged sites?

Answer 43

Eye lens proteins, heart muscle epitopes, and antigens behind the blood-brain barrier are normally hidden from immune recognition to prevent autoimmunity.

Question 44

What are examples of autoimmune diseases due to loss of tolerance?

Answer 44

Systemic lupus erythematosus, scleroderma (systemic); Graves' disease, myasthenia gravis, multiple sclerosis (organ-specific).

Question 45

How does Graves' disease cause thyroid overactivity?

Answer 45

Autoantibodies mimic TSH and stimulate the TSH receptor on thyroid cells, leading to excessive hormone production.

Question 46

What distinguishes Type I hypersensitivity reactions?

Answer 46

They are IgE-mediated, rapid in onset, involve mast cells, and can be local (e.g., eczema) or systemic (e.g., anaphylaxis).

Question 47

How does anaphylaxis occur and how is it treated?

Answer 47

Anaphylaxis is a systemic Type I reaction causing airway obstruction and hypotension; treated with epinephrine (adrenaline) pens to reverse symptoms.

Question 48

What are key diagnostic tools for allergies?

Answer 48

Skin prick tests (wheal and flare response) and blood tests (ELISA) to detect allergen-specific IgE levels.

Question 49

What distinguishes Type II hypersensitivity?

Answer 49

Involves IgG or IgM against cell-surface antigens, leading to cell lysis via complement. Examples: transfusion reaction, hemolytic disease of the newborn.

Question 50

What defines Type III hypersensitivity?

Answer 50

Formation of immune complexes between antigens and antibodies; these deposit in tissues, triggering inflammation and complement activation. Example: rheumatoid arthritis.

Question 51

What is Type IV hypersensitivity?

Answer 51

Delayed-type hypersensitivity mediated by Th1 cells, macrophages, and cytotoxic T cells; not antibody-based. Example: tuberculin skin test, nickel allergy.

Question 52

What is central tolerance and where does it occur?

Answer 52

Central tolerance is the deletion or inactivation of self-reactive B cells (in bone marrow) and T cells (in thymus) during development to prevent autoimmunity.

Question 53

What gene is critical for central tolerance in T cells?

Answer 53

The Aire gene is expressed in thymic medullary epithelial cells and enables presentation of tissue-specific antigens for deletion of autoreactive T cells.

Question 54

What is peripheral tolerance and when is it needed?

Answer 54

Peripheral tolerance is the inactivation of self-reactive lymphocytes that escape central tolerance. It occurs in tissues and is essential for preventing autoimmunity.

Question 55

What are the three mechanisms of peripheral tolerance?

Answer 55

1) Deletion (apoptosis after chronic antigen exposure), 2) Anergy (failure to respond due to lack of co-stimulation), 3) Suppression (by regulatory T cells).

Question 56

How does activation-induced cell death (AICD) contribute to tolerance?

Answer 56

Repeated T cell activation induces Fas and FasL expression, which interact to trigger apoptosis—a mechanism to delete self-reactive or overactive T cells.

Question 57

What is the role of CTLA-4 in inducing anergy?

Answer 57

CTLA-4 on T cells binds B7 on APCs with higher affinity than CD28, but without delivering an activation signal, thus promoting T cell anergy even in the presence of antigen.

Question 58

What is immune ignorance and how can it lead to autoimmunity?

Answer 58

Immune ignorance occurs when self-antigens are sequestered in immune-privileged sites and not seen by the immune system. Trauma can release these antigens, triggering an immune response.

Question 59

What is the role of Tregs in tolerance?

Answer 59

Regulatory T cells (Tregs) suppress immune responses through cytokine production (e.g., IL-10, TGF-β) and direct cell contact, helping maintain tolerance to self-antigens.

Question 60

What are the two broad classes of autoimmune diseases?

Answer 60

1) Systemic (e.g., systemic lupus erythematosus, scleroderma), 2) Organ-specific (e.g., type 1 diabetes, multiple sclerosis, Graves' disease).

Question 61

What is a key feature of Type I hypersensitivity?

Answer 61

Rapid onset (within minutes), involvement of IgE, mast cells, and basophils. Leads to symptoms like sneezing, wheezing, rashes, or anaphylaxis.

Question 62

What is a 'priming dose' in allergy?

Answer 62

The first exposure to an allergen sensitizes the immune system without causing symptoms. Upon re-exposure ('shocking dose'), the allergic reaction occurs.

Question 63

What is the immunological mechanism behind anaphylaxis?

Answer 63

Massive degranulation of mast cells releases histamine and other mediators, leading to vasodilation, bronchoconstriction, and a drop in blood pressure.

Question 64

Which antibody is involved in Type II hypersensitivity?

Answer 64

IgG or IgM bind to antigens on cell surfaces, activating complement and resulting in cell lysis. Example: hemolytic anemia.

Question 65

What is a neoantigen in drug-induced hypersensitivity?

Answer 65

A drug may bind to a normal host protein, forming a novel antigen that elicits a harmful immune response, often resembling Type II hypersensitivity.

Question 66

What is a defining feature of Type III hypersensitivity?

Answer 66

Involves immune complexes of soluble antigen and antibody, deposited in tissues causing complement activation and inflammation. Often delayed in onset.

Question 67

How does Type IV hypersensitivity cause tissue damage?

Answer 67

Mediated by CD4+ Th1 cells, CD8+ T cells, and macrophages. Leads to inflammation, granuloma formation, and delayed tissue destruction. Examples include contact dermatitis.

Question 68

What are examples of diseases caused by each type of hypersensitivity?

Answer 68

Type I: Asthma, anaphylaxis; Type II: Graves' disease, hemolytic anemia; Type III: Lupus, RA; Type IV: Contact dermatitis, type 1 diabetes.

Question 69

What are common symptoms of allergic reactions?

Answer 69

Nasal: sneezing, itching; Eyes: redness, itching; Lungs: wheezing; Skin: eczema, hives; GI: cramps, vomiting, diarrhea.

Question 70

What is the purpose of ELISA in allergy diagnosis?

Answer 70

Enzyme-linked immunosorbent assay (ELISA) detects allergen-specific IgE antibodies in the blood to diagnose Type I hypersensitivity.

Question 71

What is the clinical importance of understanding hypersensitivity in pharmacy?

Answer 71

Helps avoid drug-induced reactions, understand autoimmune pathology, and manage allergy treatments including antihistamines, steroids, and epinephrine.