Exam questions 12, 13 Flashcards

1
Q

Cytokine action on cells

A

A cytokine acts on a cell if the cell expresses the corresponding receptor. TNF binds TNFR, activating NF-κB or triggering apoptosis.

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2
Q

Cytokine response detection methods

A

qRT-PCR/PCR (mRNA detection), ELISA (protein levels), Flow Cytometry (intracellular proteins), Bioassays (functional activity).

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3
Q

IL-1β production mechanism

A

Pro-IL-1β is transcribed via NF-κB, cleaved by caspase-1, and secreted after inflammasome activation.

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4
Q

Cytokine regulation methods

A

Short half-life, decoy receptors, antagonists (e.g., IL-1Ra), post-translational modifications.

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5
Q

T lymphocytes and antigen encounter

A

T cells meet antigens in lymph nodes, transported by APCs from the infection site.

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6
Q

B vs T cell antigen recognition

A

B cells recognize native antigens, T cells recognize processed antigens on MHC.

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7
Q

B-cell activation (TD and TI antigens)

A

TD requires T-helper cell interaction, TI activates B-cells via BCR crosslinking or co-receptors.

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8
Q

Thymic T-cell selection

A

Positive selection for self-MHC recognition, negative selection to eliminate self-reactive T-cells.

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9
Q

TCR gene rearrangement

A

TCR β-chain undergoes V-DJ joining, α-chain V-J joining, RAG proteins mediate recombination, allelic exclusion.

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10
Q

MHC I and MHC II expression

A

MHC I on all nucleated cells for intracellular antigens, MHC II on APCs for extracellular antigens.

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11
Q

MHC I vs MHC II peptides

A

MHC I binds short peptides (8-10 amino acids), MHC II binds longer peptides (13-18 amino acids).

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12
Q

MHC molecules as “protein fingerprints”

A

MHC presents peptides from the cell’s protein turnover, reflecting its environment.

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13
Q

MHC molecules as “promiscuous”

A

MHC molecules bind various peptides fitting structural constraints.

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14
Q

MHC prediction algorithms

A

Based on anchor residues and peptide spacing for computational predictions.

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15
Q

KIRs on NK cells

A

KIRs inhibit NK cells by recognizing MHC I molecules

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16
Q

NK cell killing mechanism

A

NK cells induce apoptosis via perforin/granzyme release and death receptor activation.

17
Q

Cardinal signs of inflammation

A

Heat (calor), Redness (rubor), Swelling (tumor), Pain (dolor), Loss of function (functio laesa).

18
Q

Host defense in wound infection

A

Complement activation, neutrophil recruitment, cytokine release, antigen presentation, adaptive immunity activation.

19
Q

Adaptive response to mycobacteria

A

Th1 response with IFN-γ, IL-12, macrophage activation, CTL activation for infected cells.

20
Q

Desirable vaccine properties

A

Immunogenicity, long-term memory, safety.

21
Q

Adjuvant effect

A

Enhances immune response by activating PRRs and stimulating cytokine production.

22
Q

TLR-induced pathways

A

MyD88 pathway activates NF-κB for inflammation, TRIF pathway activates IRF for type I interferons.

23
Q

Autoimmune hemolytic anemia mechanism

A

Autoantibodies target RBCs

24
Q

Hypogammaglobulinemia

A

Deficiency in antibody production, leading to recurrent bacterial infections.

25
Q

Wound infection host defense steps

A

Complement activation, neutrophil recruitment, cytokine release, antigen presentation, adaptive immunity.

26
Q

LPS recognition by immune cells

A

LPS binds TLR4-MD2 complex, activating NF-κB and IRF3 for cytokine production.

27
Q

IL-1β production

A

TLR activation induces pro-IL-1β, inflammasome activation cleaves it to mature IL-1β.

28
Q

Adjuvancy explanation

A

Enhances immune response by stimulating PRRs and providing co-stimulatory signals.

29
Q

KIRs function on NK cells

A

Inhibit NK activity through MHC I recognition

30
Q

NK cell target killing mechanisms

A

Perforin/granzyme pathway and death receptor activation induce apoptosis in target cells.

31
Q

B-cell activation by thymus-dependent antigens

A

T-helper cell interaction and CD40-CD40L signaling trigger B-cell activation and differentiation.

32
Q

Antibody structure and function

A

Y-shaped structure, Fab region for antigen binding, Fc for effector functions (e.g., opsonization, complement activation).

33
Q

Class switching mechanism

A

AID deaminates cytosines, DNA breaks are repaired, leading to new antibody isotype.

34
Q

TCR diversity mechanisms

A

V(D)J recombination during T-cell development, junctional diversity via N-nucleotide addition.

35
Q

Effector T-cell subsets

A

CD4+ T-cells: Th1, Th2, Th17, Treg. CD8+ T-cells: Cytotoxic T lymphocytes (CTLs).

36
Q

Th1 vs Th2 balance

A

Th1 promotes cell-mediated immunity, Th2 promotes humoral immunity.

37
Q

Immune response against viruses

A

Th1 responses and CTL-mediated killing of infected cells.

38
Q

Type I interferons in antiviral defenses

A

Induces antiviral states, enhances NK and CTL activity, upregulates MHC I.