Exam questions 11, 16, 17

Question 1

Macrophage functions:

Answer 1

Phagocytosis, antigen presentation, cytokine production.

Question 2

TLR structure:

Answer 2

Extracellular LRRs for ligand binding, transmembrane domain, cytoplasmic TIR domain for signaling.

Question 3

TLR MyD88 signaling:

Answer 3

TLR binds PAMPs, recruits MyD88, activates IRAKs, TRAF6, TAK1, IKK, releases NF-κB to initiate cytokine transcription.

Question 4

IL-1b secretion regulation:

Answer 4

Pro-IL-1b cleaved by caspase-1 into mature IL-1b by inflammasome activation.

Question 5

Complement activation pathways:

Answer 5

Classical (C1q binding to antibodies), Lectin (MBL binding to carbohydrates), Alternative (spontaneous C3 hydrolysis).

Question 6

Complement functions:

Answer 6

MAC formation, opsonization, inflammation via anaphylatoxins.

Question 7

MAC assembly:

Answer 7

C5b binds C6, C7, C8, C9 to form a pore in pathogen membrane.

Question 8

Complement deficiency disease:

Answer 8

Hereditary angioedema, C1 inhibitor deficiency, causing excessive bradykinin release.

Question 9

Antigens:

Answer 9

Molecules recognized by the immune system, triggering an immune response.

Question 10

Antigen presentation:

Answer 10

Displaying antigen-MHC complexes on cell surfaces for T-cell recognition.

Question 11

MHCI pathway:

Answer 11

Intracellular antigens degraded by proteasome, loaded onto MHCI, recognized by CD8+ T cells.

Question 12

MHCII pathway:

Answer 12

Extracellular antigens endocytosed, processed, and loaded onto MHCII, recognized by CD4+ T cells.

Question 13

Naïve CD8+ T-cell priming:

Answer 13

Dendritic cells present antigen via MHCI, CD4+ T cells “license” dendritic cells.

Question 14

Primary foci vs germinal centers:

Answer 14

Primary foci produce low-affinity antibodies quickly, germinal centers undergo somatic hypermutation and class switching for high-affinity antibodies.

Question 15

Germinal center processes:

Answer 15

Somatic hypermutation (SHM) improves antigen binding, class-switch recombination (CSR) changes antibody isotype.

Question 16

Antibody effector functions:

Answer 16

Fc region mediates neutralization, complement activation, opsonization, ADCC.

Question 17

ADCC vs T-cell-mediated cytotoxicity:

Answer 17

ADCC: NK cells, antibodies bind to infected cells. T-cell: CD8+ T cells recognize antigens via MHCI.

Question 18

Monoclonal vs polyclonal antibodies:

Answer 18

Monoclonal: One epitope, high specificity. Polyclonal: Multiple epitopes, broader detection.

Question 19

Linear vs conformational determinants:

Answer 19

Linear: Recognized by amino acid sequence. Conformational: Recognized by 3D protein structure.

Question 20

Leukocyte types and functions:

Answer 20

Neutrophils: Phagocytosis, first responders. Basophils: Release histamine, allergies. Eosinophils: Combat parasites. Monocytes: Differentiate into macrophages or dendritic cells.

Question 21

Physical and chemical barriers:

Answer 21

Skin, mucous membranes prevent pathogen entry

Question 22

Monoclonal and polyclonal antibody definitions:

Answer 22

Monoclonal: One epitope, high specificity. Polyclonal: Multiple epitopes, broader detection.

Question 23

Pros/Cons of monoclonal antibodies:

Answer 23

Pros: Specific, reproducible. Cons: Expensive, may miss heterogeneity.

Question 24

Enzyme-Linked ImmunoSorbent Assay (ELISA):

Answer 24

Detects antigens/antibodies using enzyme-linked antibodies for color change. Clinical use: HIV antibody detection, pregnancy tests.

Question 25

MHC molecule display:

Answer 25

MHCI: Intracellular peptides, recognized by CD8+ T-cells. MHCII: Extracellular peptides, recognized by CD4+ T-cells. CD1: Lipid-based antigens, recognized by specific T-cells.

Question 26

MHCI/MHCII antigen presentation:

Answer 26

MHCI: Intracellular antigen processing via proteasome, ER transport. MHCII: Extracellular antigen processing in endosomes.

Question 27

Cross-priming:

Answer 27

Dendritic cells present extracellular antigens on MHCI, activating CD8+ T-cells.

Question 28

Naïve T-cell activation:

Answer 28

Signal 1: TCR binding, Signal 2: Co-stimulation (CD28/B7), Signal 3: Cytokines for differentiation.

Question 29

T-cell subsets and cytokines:

Answer 29

Th1: IFN-γ, macrophage activation. Th2: IL-4, IL-13, B-cell activation. Th17: IL-17, inflammation. Treg: IL-10, TGF-β, immune suppression. CD8+ T-cells: Kill infected cells via perforin/granzymes.

Question 30

Cancer hallmarks:

Answer 30

Sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling immortality, inducing angiogenesis, activating invasion/metastasis, avoiding immune destruction.

Question 31

Proto-oncogenes vs tumor suppressor genes:

Answer 31

Proto-oncogenes promote growth

Question 32

Tumor-specific vs tumor-associated antigens:

Answer 32

Tumor-specific: Unique to tumor cells. Tumor-associated: Overexpressed in tumors but also present in normal cells.

Question 33

B-cell activation by thymus-dependent antigens:

Answer 33

Antigen binding activates B-cells, interaction with CD4+ T-cells for proliferation, SHM, and CSR, forming plasma and memory cells.

Question 34

Apoptosis:

Answer 34

Programmed cell death, intrinsic pathway activates caspases, apoptotic debris cleared by phagocytes.

Question 35

Phagocytosis process:

Answer 35

Binding, uptake into phagosomes, fusion with lysosomes, degradation and presentation.

Question 36

Importance of phagocytosis:

Answer 36

Removes pathogens, processes antigens for T-cell presentation.

Question 37

Phagocytosing cells:

Answer 37

Macrophages, neutrophils, dendritic cells, monocytes.

Question 38

Direct vs indirect phagocytosis activation:

Answer 38

Direct: PRRs bind microbes. Indirect: Opsonins mark microbes for phagocytosis.

Question 39

Antigen presentation and adaptive immunity:

Answer 39

Antigen presentation activates T-cells, initiating immune responses.

Question 40

MHCII expression and recognition:

Answer 40

MHCII on dendritic cells, macrophages, B-cells

Question 41

Cytosolic antigen processing:

Answer 41

Degraded by proteasomes, loaded onto MHCI, presented to CD8+ T-cells.

Question 42

CD8+ T-cell priming:

Answer 42

Cross-presentation by dendritic cells using MHCI.

Question 43

CD4+ T-cell activation signals:

Answer 43

TCR recognition, co-stimulation, cytokines for differentiation.

Question 44

Cytotoxic T cells and NK cells killing mechanism:

Answer 44

Perforin-granzyme pathway, Fas-FasL interaction (CTL only), NK cells also mediate ADCC.

Question 45

Cytotoxic T cells vs NK cells target identification:

Answer 45

CTLs recognize MHCI-presented antigens, NK cells detect absence of MHCI or antibody-coated targets.

Question 46

CD4+ T helper subsets:

Answer 46

Th1, Th2, Th17, Tfh, Treg.

Question 47

Th1 and Th2 cytokine roles:

Answer 47

Th1: IFN-γ for macrophage activation. Th2: IL-4, IL-5 for B-cell activation.

Question 48

Mature naïve B-2 cell characteristics:

Answer 48

Surface IgD, IgM, recirculates between blood and lymphoid organs, expresses CD19, CD21, CD40.

Question 49

Antibody structure:

Answer 49

Y-shaped glycoproteins with heavy and light chains, variable region for antigen binding, constant region for effector function.

Question 50

T-dependent B-2 cell response:

Answer 50

Antigen binding, presentation to CD4+ T-cells, proliferation, SHM, CSR, differentiation into plasma and memory cells.

Question 51

IgM and IgG complement activation:

Answer 51

Both recruit C1q, IgM is more effective due to pentamer structure.

Question 52

B-1 vs T-dependent B-2 cell antibodies:

Answer 52

B-1: IgM, low affinity. B-2: High-affinity, isotype-switched, SHM, and CSR.

Question 53

BCR structure:

Answer 53

Immunoglobulin with hydrophilic spacer, hydrophobic transmembrane region, cytoplasmic tail.

Question 54

Igα/Igβ signaling from BCR:

Answer 54

Phosphorylation of ITAM motifs, recruitment of adaptor proteins.

Question 55

Phospholipid modification leading to Ca²⁺ increase:

Answer 55

PLCγ cleaves PIP2, producing DAG and IP3, which increase cytosolic Ca²⁺.

Question 56

Increased Ca²⁺ and NFAT activation:

Answer 56

Ca²⁺ binds calmodulin, activating calcineurin, dephosphorylates NFAT for nuclear translocation.