Exam questions 18, 19 Flashcards

1
Q

Innate immune cell types and roles

A

Macrophages: Phagocytose microbes and debris, present antigens, and release cytokines. Dendritic cells: Capture and process antigens, present antigens to T cells, linking innate and adaptive immunity. Neutrophils: Phagocytose pathogens and release bactericidal substances. NK cells: Kill virus-infected and cancerous cells via lytic granules. Mast cells: Release histamine and other inflammatory mediators, promoting allergic reactions and parasitic defense.

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2
Q

Complement system activation pathways

A

Classical: C1q binds antibody-antigen complexes. Lectin: Mannose-binding lectin binds microbial carbohydrates. Alternative: Spontaneous C3 hydrolysis or C3b binding to pathogens.

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3
Q

C5 cleavage in complement system

A

C5a: Inflammatory mediator, recruits immune cells. C5b: Initiates membrane attack complex (MAC) formation, leading to pathogen lysis.

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4
Q

Pattern-recognition receptors (PRRs) families

A

TLRs, NLRs, CLRs, RLRs, CDSs.

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5
Q

PRRs sensing double-stranded RNA

A

RIG-I/MDA5: Cytosolic, signals through MAVS, induces IFN-β and antiviral responses. TLR3: Endosomal, signals through TRIF, induces IFN-β and antiviral responses.

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6
Q

Naïve CD4+ T helper cell activation

A

Antigen-presenting cells present antigens via MHC II to CD4+ T cells, initiating signaling through TCR and CD4 co-receptor.

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7
Q

CD4+ T cell subsets and cytokines

A

IL-12 + IFN-γ: Th1 IL-6 + IL-23: Th17 IL-4: Th2 TGF-β + IL-2: Treg IL-6: Tfh

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8
Q

Main functions of CD4+ T helper subsets

A

Th1: Activates macrophages, fights intracellular pathogens. Th17: Inflammation, defense against bacteria and fungi. Th2: Helps in parasitic immunity and antibody production. Treg: Suppresses immune responses, maintains tolerance. Tfh: Supports B cell activation and antibody production.

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9
Q

Licensing dendritic cells to activate CD8+ T cells

A

Dendritic cells present extracellular antigens via MHC I, providing co-stimulatory signals to activate CD8+ T cells.

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10
Q

Viral evasion via TAP inhibition

A

Inhibition of TAP prevents MHC I antigen presentation, impairing CD8+ T cell activation, but enhances NK cell-mediated killing.

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11
Q

Cytotoxic T cells, NK cells, NKT cells recognition

A

Cytotoxic T cells: Recognize antigens on MHC I. NK cells: Detect absence of MHC I or antibody-coated targets. NKT cells: Recognize lipid antigens presented on CD1d.

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12
Q

V(D)J recombination enzymes

A

RAG1/2: Initiates recombination at signal sequences. TdT: Adds random nucleotides, increasing diversity.

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13
Q

Follicular B2 cell activation and linked-recognition

A

B2 cells bind antigen, present it on MHC II to T helper cells. Linked-recognition requires T cell and B cell to recognize the same antigen.

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14
Q

AID processes and antibody effects

A

Somatic hypermutation (SHM): Introduces mutations in variable region, improving affinity. Class switch recombination (CSR): Changes antibody isotype for specialized functions.

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15
Q

Antibody isotypes

A

IgM, IgD, IgG, IgA, IgE.

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16
Q

Antibodies promoting phagocytosis

A

Antibodies activate complement (C3b), opsonize microbes for phagocyte recognition.

17
Q

FcεRI signaling mutation effects

A

Impaired IgE signaling increases susceptibility to parasitic infections and reduces allergic reactions.

18
Q

Monoclonal vs polyclonal antibodies

A

Monoclonal: Specific to one epitope, from a single B cell clone. Polyclonal: Recognize multiple epitopes, from multiple B cells.

19
Q

Secondary/acquired immunodeficiency

A

Caused by external factors, such as infections (e.g., HIV) or cancer.

20
Q

Herd immunity

A

Protection occurs when a large portion of the population is immune, reducing disease spread.

21
Q

Immune response phases toward infection

A

Innate: Rapid, involves antimicrobial proteins, phagocytes, complement, and NK cells. Adaptive: Involves T and B cell activation, differentiation into effector cells, and memory formation.

22
Q

Phagocytosis process and phagocytes

A

Phagocytosis: Engulfing pathogens into phagosomes for degradation. Neutrophils: Rapid responders, kill pathogens via granules. Macrophages: Resident cells, phagocytose pathogens, present antigens.

23
Q

Role of C3 in immune response

A

C3 is essential for complement activation, opsonization, inflammation, and pathogen lysis. C3 deficiency: Increased susceptibility to bacterial infections and inability to form MAC.

24
Q

Dendritic cells bridging innate and adaptive immunity

A

Dendritic cells capture pathogens and present antigens to T cells, providing co-stimulatory signals to initiate adaptive immunity.

25
Q

MHC I and MHC II expression and antigen loading

A

MHC I: Expressed on all nucleated cells, presents intracellular antigens to CD8+ T cells. MHC II: Expressed on professional APCs, presents extracellular antigens to CD4+ T cells.

26
Q

Positive selection of thymocytes and self-MHC restriction

A

Positive selection: Thymocytes that bind self-MHC with moderate affinity survive and differentiate. Self-MHC restriction: T cells recognize antigens only when presented by self-MHC molecules.

27
Q

AIRE mutation and autoimmune disorders

A

AIRE allows tissue-specific antigen presentation in the thymus for self-tolerance. Its loss leads to autoimmune diseases.

28
Q

HIV infection and CD4+ T cell loss

A

Loss of CD4+ T cells impairs adaptive immunity, leading to susceptibility to infections and loss of effective immune responses.

29
Q

Th1 characteristics and role in immune response

A

Induced by IL-12 and IFN-γ, Th1 cells produce IFN-γ, activating macrophages for intracellular pathogen destruction.

30
Q

Hematopoietic stem cells

A

Hematopoietic stem cells give rise to all blood cells, with self-renewal and multipotency abilities.

31
Q

Antibody diversity in B2 cells

A

Combinatorial diversity, heavy-light chain pairing, P-nucleotide addition, exonuclease trimming, N-nucleotide addition by TdT.

32
Q

Class-switch rearrangement importance

A

Enables antibodies to perform specialized functions by switching isotypes like IgG, IgA, and IgE.

33
Q

IgM vs IgA structure and function

A

IgM: Pentameric, efficient complement activation, cannot cross placenta. IgA: Predominant in mucosal secretions, neutralizes pathogens without complement activation.

34
Q

Types of vaccines and their advantages/disadvantages

A

Live attenuated: Pro - Strong immune response, fewer boosters. Con - Risk of reversion. Inactivated: Pro - Safe, stable storage. Con - Requires boosters, weak cell-mediated immunity. Subunit: Pro - Safe, stable. Con - Requires adjuvants and boosters.