13 - Effector Responses Flashcards

1
Q

What are the effector molecules of humoral immunity?

A

antibodies

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2
Q

What are the effector cells of the cell-mediated immunity?

A

CTLs

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3
Q

What are the ways that humoral immunity is carried out?

A

neutralization | opsonization | agglutination | complement activation | antibody-dependent cell-mediated cytotoxicity (ADCC) | degranulation

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4
Q

What is the neutralization aspect of humoral immunity?

A

neutralizes toxins, pathogens, or proteins and blocks them from doing its job

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5
Q

What is the agglutination aspect of humoral immunity?

A

antigen/antibody complex enhances neutralization and clearance from body

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6
Q

What is the opsonization aspect of humoral immunity?

A

antibody bound to pathogen also binds to Fc receptor = macrophage will recognize this complex (due to FcR) and phagocytose pathogen

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7
Q

What is the complement activation aspect of humoral immunity?

A

involves MAC complex

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8
Q

What is the antibody-dependent cell cytotoxicity aspect of humoral immunity?

A

activates NK cells and CTLs

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9
Q

What is the degranulation aspect of humoral immunity?

A

Fc receptor-mediated | IgE degranulates granulocytes to release contents onto pathogen

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10
Q

What are the 5 characteristics of IgM?

A

first Ab activated | pentamer if secreted | membrane-bound on B-cells | lower affinity to antigen = 10 Ag binding sites | activates complement

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11
Q

What are the main roles of IgM?

A

opsonization | antigen/antibody complex formation

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12
Q

What are the characteristics of IgG?

A

only one to cross placenta | most prominent | all bind to Fc receptors

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13
Q

What are the 3 main roles of IgG?

A

activate macrophages | induce complement | mediates cell cytotoxicity (ADCC)

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14
Q

What are the 6 characteristics of IgA?

A

found in mucosal secretions | not fix complement = no inflammation | protease-resistant | dimer | not bind to FcR | mom passes this Ab on to fetus

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15
Q

What are the 2 main roles of IgA?

A

neutralizes toxins/pathogens | cross mucosal surfaces

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16
Q

What are the 6 characteristics of IgE?

A

allergy and worm infections | asthma |

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17
Q

What is the main role of IgE?

A

degranulation of granulocytes = release molecules to damage large pathogens

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18
Q

What are the 6 characteristics of IgD?

A

least common | membrane-bound and secreted | present in upper lung secretions

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19
Q

What are the 2 main roles of IgD?

A

binds basophils and mast cells | stimulates release of antimicrobial peptides

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20
Q

What is the function of Fc receptors?

A

induce effector reaction onto cell via signaling cascade

21
Q

How are FcRs activated?

A

antibody binding and FcRs need to be “cross-linked” (bringing in multiple FcRs together)

22
Q

What do FcRs use to initiate a signaling cascade and why?

A

ITAM and ITIM regions | don’t have a cytoplasmic tail region

23
Q

What do ITAMs do?

A

induces phosphorylation of certain regions

24
Q

What are ITIMs?

A

suppress immune responses of the co-receptors for FcRs

25
Q

Which part of the antibody carries out the immune response? What is it determined by?

A

constant region = determined by antibody isotype

26
Q

What is a key feature of FcRs that helps antibodies stick to them?

A

immunoglobulin domains

27
Q

Where are PolyIgR expressed?

A

expressed on epithelial cells (not immune cells)

28
Q

What are the 3 characteristics of Fc-gamma-R?

A

most diverse FcRs | binds to IgG | most are activating receptors = ITAMS

29
Q

What is the main role of FcgR?

A

induce phagocytosis

30
Q

What are the characteristics of FceR?

A

binds to IgE | ONLY found on mast cells/eosinophils/basophils

31
Q

What is the main role of FceR?

A

degranulation of granulocytes

32
Q

What happens if there is no pathogen to dump the granule contents onto during an allergic response?

A

contents will be dumped onto your tissues = causes inflammation

33
Q

What is the main role of PolyIgR?

A

transports IgA and IgM from blood to tissues or lumen of tissues

34
Q

What is FcRn?

A

neonatal receptor that helps IgG cross placental barrier

35
Q

What is the 2nd signal needed for CTL activation?

A

CD28

36
Q

What 2 genes does cytokine signaling of IL2 lead to the expression of?

A

Bcl-2 (pro-survival gene) | CD25 (IL2R)

37
Q

What are the 2 ways in which CTLs can kill infected/tumor cells?

A

intrinsic pathway | extrinsic pathway

38
Q

What is the intrinsic pathway of CTLs?

A

produce protein to insert into infected/tumor cell

39
Q

What are the 2 key proteins in the intrinsic pathway of CTLs?

A

perforins | granzymes

40
Q

What are perforins?

A

pore-forming protein

41
Q

What are granzymes?

A

proteases that turn on caspase (apoptotic) molecules

42
Q

What is the extrinsic pathway of CTLs?

A

engages the Fas/FasL CTL ligand with the FasR receptor on target cell = interaction activates caspase = activates apoptosis

43
Q

How do CTLs insert apoptotic proteins into target cell?

A

perforin and granzyme = exocytosed &raquo_space;> target cell endocytoses them &raquo_space;> perforin makes a pore on endocytic vesicle to let granzymes out = activate caspase = induce apoptosis

44
Q

What is the missing self model of NK cells?

A

NK cells recognize and kill infected/tumor cells by absence of MHC I

45
Q

How do NK cells interact with normal cells?

A

normal cells have both NK activating ligand AND MHC I ligands

46
Q

If a cell presents more MHC I than activating ligand, what does the NK cell do?

A

over-representation of MHC I will bind to more inhibitory receptors on NK cell = NK-cell inhibition

47
Q

If a cell presents less/no MHC I and has more activating ligands, what does the NK cell do?

A

under-representation or no expression of MHC I = less binding of inhibitory receptor and more binding of activation receptor = NK cell activation = target cell dies

48
Q

If a cell has an equal number of MHC I and activating ligand, what does the NK cell do?

A

nothing happens

49
Q

What does “missing self” mean?

A

the loss of ability to express self-protein (ie: MHC I) on cell surface