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BIOM2011 > Immunology 2025 > Flashcards

Immunology 2025 Flashcards

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1
Q

What are the primary functions of the immune system?

A

To protect against invasion by foreign organisms through both innate and adaptive immunity.

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2
Q

List the components of innate immunity.

A

Macrophages, granulocytes, NK cells, complement, and physical barriers.

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3
Q

What are the main features of adaptive immunity?

A

Involves T and B cells, highly specific, has memory, and improves upon repeated exposure.

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4
Q

What are examples of physical barriers in the immune system?

A

Skin and mucosal surfaces.

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4
Q

Compare the innate and adaptive immune responses in terms of speed and memory.

A

Innate is rapid (hours), lacks memory; adaptive is slower (days) but has memory and improved response upon re-exposure.

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5
Q

What are the four classic signs of inflammation?

A

Rubor (redness), calor (heat), tumor (swelling), and dolor (pain).

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6
Q

What vascular changes occur during inflammation?

A

Vasodilation, adhesion molecule expression, and increased vascular permeability.

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7
Q

What are PAMPs and how do they relate to innate immunity?

A

Pathogen-Associated Molecular Patterns are recognized by receptors (like TLRs), triggering inflammation

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8
Q

Name some types of tissue macrophages and their roles.

A

Microglia: Phagocytose dying neurons

Alveolar macrophages: Respond to irritants

Spleen macrophages: Clear dying cells/particulates

Kupffer cells: Gut-derived microbial exposure

Joint macrophages: Inflammatory cytokines in arthritis

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9
Q

What are the four main stages of phagocytosis?

A

Binding to receptors

Engulfment

Phagosome-lysosome fusion

Killing and degradation

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10
Q

Why do tattoos persist in the skin?

A

Macrophages phagocytose ink particles and when they die, new macrophages take up the ink, maintaining colour.

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11
Q

What is the primary function of neutrophils?

A

Phagocytosis and killing of pathogens, especially during acute inflammation.

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12
Q

What is chemotaxis in the immune response?

A

Movement of immune cells toward the source of chemokines or other attractants.

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13
Q

What are the functions of the complement system?

A

Recruitment of inflammatory cells

Killing of pathogens

Opsonization (coating microbes for enhanced phagocytosis)

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14
Q

What triggers mast cell activation?

A

IgE binds mast cells; upon allergen exposure, crosslinking of FcεRI receptors leads to degranulation.

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14
Q

How is the complement system activated?

A

By a cascade of plasma proteins (C1–C9) that assemble on microbial surfaces.

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15
Q

What immune conditions involve mast cells and basophils?

A

Type I hypersensitivity reactions, including allergic responses and certain parasite infections.

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16
Q

What are NK (Natural Killer) cells and their function?

A

Lymphoid cells that kill virus-infected or tumor cells by detecting the absence of MHC I.

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17
Q

What is ADCC in NK cell function?

A

Antibody-Dependent Cell-Mediated Cytotoxicity – antibodies bind to target cells, activating NK cells via Fc receptors.

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18
Q

How is NK cell activation controlled?

A

By a balance between activating and inhibitory receptor signals; lack of MHC I tips the balance toward activation.

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19
Q

Summarize the acute inflammatory response.

A

It involves detection of pathogens, recruitment of immune cells (via chemotaxis), phagocytosis, complement activation, and inflammation leading to pathogen elimination.

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20
Q

What disease is an example of impaired mucosal defence?

A

Cystic Fibrosis – due to thick mucus and reduced clearance, increasing infection risk.

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21
Q

How does innate and adaptive immunity respond to repeat infection?

A

Innate response is the same as the primary; adaptive response is faster and stronger due to memory.

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22
Q

What is chemotaxis?

A

Movement of immune cells up a concentration gradient toward the source of chemoattractants.

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23
Which immune cells are involved in acute inflammation?
Neutrophils (predominantly), macrophages, and mast cells
24
What attracts neutrophils to sites of infection?
Chemokines and complement-derived factors.
25
Which cells perform phagocytosis?
Neutrophils, macrophages, and dendritic cells.
26
Q: What role do TLRs (Toll-Like Receptors) play in phagocytosis?
They help recognize pathogens via PAMPs, activating phagocytes.
27
How do NK cells recognize infected cells?
They detect the absence of MHC I, or are activated by antibody-bound cells via Fc receptors (ADCC).
28
What is ADCC in NK cell function?
Antibody-dependent cell-mediated cytotoxicity – antibodies activate NK cells to kill target cells.
29
How do T cells recognize antigens?
T cells recognize processed peptides presented by MHC molecules on the surface of antigen-presenting cells (APCs).
30
What is the role of MHC molecules in antigen presentation?
MHC molecules bind peptide fragments and present them to T cell receptors (TCRs).
31
What is the origin of peptides presented by MHC Class I?
Cytosolic proteins degraded by the proteasome; peptides are transported into the ER by TAP and loaded onto MHC I.
32
What is the origin of peptides presented by MHC Class II?
Extracellular or vesicle proteins taken up by endocytosis, degraded in acidified endosomes, and loaded onto MHC II in vesicles.
33
Which MHC class presents to which T cell type?
MHC I → CD8 T cells MHC II → CD4 T cells
34
What is the function of CD8+ T cells?
Cytotoxic T lymphocytes (CTLs) that kill virally infected or abnormal cells via perforin and granzyme release.
35
What is the function of CD4+ T cells?
Helper T cells that secrete cytokines to activate macrophages, help B cells, and regulate immune responses.
36
What does the CD8 TCR recognize?
Peptides presented by MHC Class I molecules.
37
What does the CD4 TCR recognize?
Peptides presented by MHC Class II molecules.
38
Name the CD4+ T cell subsets and their roles.
Th1: Activates macrophages (via IFN-γ) Tfh/Th2: Help B cell activation and antibody production Th17: Promotes inflammation Treg: Suppresses immune responses
39
Where do T cells develop?
In the thymus, after originating from bone marrow precursors.
40
What is T cell selection?
A process in the thymus where T cells with high affinity for self MHC/peptide are deleted (negative selection).
41
What is the purpose of T cell selection
To ensure self-tolerance and prevent autoimmunity by eliminating self-reactive T cells.
42
Where do naïve T cells become activated
In secondary lymphoid organs (e.g., lymph nodes) after encountering antigen-presenting dendritic cells.
43
What are the two signals required for T cell activation?
TCR binding to peptide-MHC Co-stimulatory signal from APCs (e.g., CD80/86 binding to CD28)
44
What happens after T cell activation
T cells proliferate, differentiate into effector cells, and upregulate adhesion molecules and chemokine receptors.
45
How do dendritic cells contribute to T cell priming?
After activation by danger signals, they migrate to lymph nodes, stop antigen uptake, and express co-stimulatory molecules.
46
What is an antigen?
Any substance that can be specifically recognized by an antibody or BCR (B cell receptor).
47
Q: What is an epitope?
A: The specific part of the antigen that is recognized and bound by an antibody.
48
Q: What are antibodies also called?
A: Immunoglobulins (Ig).
49
Q: What happens when a BCR recognizes its antigen?
A: The B cell differentiates into a plasma cell and secretes antibodies with the same specificity.
50
Q: What is the basic structure of an antibody?
A: Two identical heavy chains and two identical light chains forming a Y-shaped molecule.
51
Q: What determines the antibody's isotype?
A: The heavy chain class (e.g., IgG, IgM, IgA, IgE, IgD).
52
Q: What types of light chains can antibodies have?
A: Kappa or lambda.
53
Q: Which antibody isotypes can form multimers?
A: IgM (pentamer) and IgA (dimer).
54
Q: Which antibody is produced first during a primary immune response?
IgM
55
Q: Which antibody dominates the secondary response?
A: IgG (or IgA depending on location), with higher affinity and more rapid production.
56
Q: How does the secondary immune response differ from the primary?
A: It is faster, stronger, and more specific due to memory B cells.
57
Q: What is isotype switching?
A: The process where B cells change from producing IgM to other antibody isotypes like IgG, IgA, or IgE.
58
Q: What triggers isotype switching?
A: Signals from helper T cells and cytokines.
59
Name 4 mechanisms generating antibody diversity.
V(D)J recombination Junctional diversity Heavy/light chain pairing Somatic hypermutation
60
Q: What are T cell-dependent antibody responses?
A: B cell activation and isotype switching that require help from CD4+ T cells.
61
Q: How do T cells assist B cells?
A: By providing cytokines and surface signals (e.g., CD40L-CD40 interaction).
62
Q: Are there T cell-independent antibody responses?
A: Yes, but they mainly produce IgM with less diversity and no memory.
63
Q: What are the five main effector functions of antibodies?
Neutralization Opsonization Complement activation Antibody-dependent cell-mediated cytotoxicity (ADCC) Triggering degranulation (mast cells, eosinophils, etc.)
64
Q: What is the main antibody in primary immune responses?
A: IgM.
65
Q: Which antibody crosses the placenta?
A: IgG.
66
Which antibody is key for mucosal immunity?
A: IgA.
67
Which antibody mediates allergic responses?
IgE.
68
Q: What is known about IgD function?
A: Its function is not well understood.
69
What are polyclonal antibodies?
A: A mixture of antibodies made by different B cells, recognizing multiple epitopes of an antigen.
70
Q: What are monoclonal antibodies?
A: Antibodies from a single B cell clone with specificity for one epitope.
71
Q: How are monoclonal antibodies produced?
A: By fusing B cells with myeloma cells to create hybridomas.
72
Q: List common research techniques using antibodies.
Immunofluorescence microscopy Immunohistochemistry Immunoprecipitation Immunoblotting Flow cytometry Magnetic bead purification
73
Q: What allows antibodies to be powerful research tools?
A: Their high specificity for particular antigens or epitopes.
74
What is primary immunodeficiency?
A genetic disorder that impairs the immune system, usually hereditary.
75
Q: What is secondary immunodeficiency?
A: An immune deficiency resulting from another disease or condition.
76
Q: Give an example of a T cell primary immunodeficiency.
A: TAP mutations reduce CD8 T cells due to impaired peptide loading on MHC I.
77
Q: Give an example of a B cell primary immunodeficiency.
A: Hyper IgM syndrome—failure of isotype switching due to defective T-B cell interaction.
78
Q: List causes of secondary immunodeficiency.
A: Burns, leukemia, chemotherapy, transplant immunosuppression, HIV.
79
What is Type I hypersensitivity?
Immediate allergic reaction involving IgE and mast cells (e.g., hay fever).
80
Q: What clinical tests are used for Type I hypersensitivity?
A: Skin prick test and skin patch test.
81
Q: What distinguishes Type II hypersensitivity?
A: Antibody-mediated cytotoxicity (IgG/IgM against cell surface antigens).
82
Q: What is Type III hypersensitivity?
A: Immune complex-mediated inflammation (e.g., serum sickness).
83
Q: What is Type IV hypersensitivity?
A: Delayed-type, T cell-mediated response (e.g., contact dermatitis).
84
Q: What is autoimmunity?
A: An immune response against self-antigens due to tolerance breakdown.
85
What are the mechanisms that prevent autoimmunity?
Central tolerance (negative selection in thymus) Antigen segregation Peripheral anergy Regulatory T cells Clonal exhaustion
86
Give examples of autoimmune diseases.
Type 1 diabetes (pancreatic β-cell destruction) Multiple sclerosis (myelin sheath destruction) Rheumatoid arthritis (synovial lining destruction)
87
Q: What is immune surveillance?
A: The immune system's role in detecting and destroying abnormal cells.
88
Q: What types of tumour antigens are recognized by the immune system?
Mutated proteins Re-expressed developmental antigens Differentiation antigens (e.g., Tyrosinase) Modified self-antigens (e.g., mucin) Oncoviral proteins (e.g., HPV)
89
Q: How do tumours escape immune detection?
A: By downregulating antigens, secreting immunosuppressive factors, or inducing T cell exhaustion.
90
Q: What are examples of cancer immunotherapies?
PAMPs to activate innate immunity Cytokine therapy (e.g., interferons) Monoclonal antibodies Cytotoxic T cell transfer Vaccines (e.g., HPV vaccine)

BIOM2011 (19 decks)

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