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Immuno > exam II > Flashcards

exam II Flashcards

1
Q

type I hypersensitivity: etiology

A

genetics, environmental exposure

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2
Q

type I sensitization

A
  1. enzyme Der P 1 cleaves tight junctions, diffuses into mucosa. Der P 1 taken up by dendritic cells for antigen presentation
  2. dendritic cell primes T cell in lymph node, Tfh and TH2 induces B-cell class switch to IgE production w/ IL-4
  3. IgE specific for Der P 1 travels to mucosa, IgE binds to FcER1 receptor on mast cell
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3
Q

type I: FcER1 binding

A

binding IgE is the tightest of all interactions (irreversible), is found in mast cells, eosinophils, basophils

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4
Q

type I: mast cell activation

A

IgE binds mast cell in absence of antigen, leads to rapid degranulation
Mast cell activation requires cross linking of FcR-bound IgE to same allergen (multiple IgE bind epitopes)

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5
Q

mast cell soluble products: toxic mediators

A

histamine and heparin increase vascular permeability, smooth muscle contraction
histamine is an early mediator, binds histamine receptors on vascular endothelium, smooth muscle, epithelium

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6
Q

mast cell soluble products: cytokines

A

Late mediators, after degranulation
IL-4, IL-13 stimulate and amplify TH2 response
IL-5 induces eosinophil production, activation

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7
Q

mast cell soluble products: lipid mediators

A

leukotrienes: similar to histamine, more potent
- increase vascular permeability, smooth muscle contraction, mucus secretion

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8
Q

type I: eosinophils

A
  • not tissue resident, circulate in low numbers
  • recruited to site or generated
  • granules are highly toxic, can damage host, produce cyto/chemokines
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9
Q

type I: basophils

A
  • low numbers in circulation, also recruited
  • express CD40L, help activated B cells class switch to IgE, IL-13, activate inactive B cells
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10
Q

RIST

A

radioimmunosorbent test quantifies total IgE in serum: not for verifying allergen types

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11
Q

RAST

A

radioallergosorbent test used to ID allergen-specific IgE

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12
Q

type I treatments

A

epinephrine: vasoconstrictor, bronchodilator
anti-histamine: blocks histamine binding to HI receptors
corticosteroids: general leukocyte inhibitors

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13
Q

type II hypersensitivity: etiology

A

antibody driven, typically IgG

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14
Q

type II: triggers

A

haptens: nonimmunogenic small molecules that modify host cell surface proteins
molecular mimicry: AB specifically generated against pathogen antigen, reactive against host antigens
autoimmunity: loss of tolerance to self-antigens

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15
Q

type II: small molecule drugs

A

ex) penicillin modifies proteins on human RBCs to create foreign epitopes, IgG made against new antigen
Complement-coated penicillin modified erythrocytes are phagocytosed, macrophages present peptides to CD4 T cells to differentiate into Tfh

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15
Q

type II: cytotoxic effector phases

A

complement fixation, opsonization/phagocytosis, ADCC mediated by NK

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16
Q

type II: non-cytotoxic effector phase

A

receptor-ligand interference

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17
Q

type III: etiology

A
  • body fails to clear immune complexes, which deposit in vessels and cause inflammation
  • antigens present in excess, large antigens w/ multiple epitopes fix complement
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18
Q

type III: effector mechanisms

A

complement fixation, FcyR mediated binding leads to histamien release and inflammation

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19
Q

type IV etiology

A
  • T cells cause pathology
  • contact: haptens, metals modify internal proteins to activate T cells
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20
Q

type IV: effector phase

A

CD4 Th1, Th17 recognize antigens, release mediators that recruit and activate inflammatory cells

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21
Q

type IV: chemokines function

A

macrophage recruitment

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22
Q

type IV: IFN-y function

A

macrophage activation

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23
Q

type IV: TNF-a function

A

local tissue destruction, increased adhesion molecules on blood vessels

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24
Q

type IV: IL-3 function

A

monocyte production

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25
Q

autoimmunity

A

immune reactivity against self-antigens resulting from a break in self-tolerance

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26
Q

autoimmunity: central tolerance breakdown related to T cells

A

-Autoreactive T cells gain access to immune-privileged sites/cryptic antigens, autoreactive T cells escape

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27
Q

tolerance

A

immune system ignores or induces tolerogenic response so self-antigens don’t elicit inflammatory response
- central: fine-tuning B, T cell receptors
- peripheral: anergy, Treg suppression, cryptic antigens

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28
Q

autoimmunity: peripheral tolerance breakdown anergy

A

T and B cells recognize antigen w/o costimulation –> become unresponsibe

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29
Q

autoimmunity: central tolerance breakdown due to genetic defect

A

Genetic defect: AIRE deficiency causes multi-organ autoimmune condition involving both B and T cells

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30
Q

autoimmunity: peripheral tolerance breakdown immune privilege

A

barriers to prevent leukocyte entry broken down, inflammation occurs

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31
Q

autoimmunity: peripheral tolerance breakdown Tregs

A

recognize self-antigen, send signals to suppress T cell responses to same antigen

32
Q

primary immunodeficiency etiology

A

inherited or acquired gene defect, can be autosomal or x-linked

33
Q

primary immunodeficiency: complement defect

A
  • classical pathway: impaired clearance of immune complexes, infection by pyogenic bacteria
  • alternative pathway defect: infection by N. gonorrhoeae, N. meningintidis
  • Masp-2 deficiency: infection by S. pneumoniae
34
Q

enumeration: T cells

A

CD4, CD8, CD3

35
Q

enumeration: B cells

A

CD20, Ig+

36
Q

enumeration: phagocytes

A

neutrophils

37
Q

assessment of in vitro functioning: T cells

A

IL-2 production, antigen-specific stimulation

38
Q

assessment of in vitro functioning: phagocytes

A

NBT test for ROS

39
Q

assessment of in vitro functioning: complement

A

hemolysis assay

40
Q

assessment of in vivo functioning: T cells

A

delayed HS to PPD of tuberculosis

41
Q

assessment of in vivo functioning: B cells

A

specific antibody levels

42
Q

cytotoxic drugs immunodeficiency

A
  • chemotherapy targets rapidly-dividing cells
  • restricts stem cells
43
Q

radiation immunodeficiency

A
  • restricts stem cells, inhibits lymphocyte proliferation
44
Q

immunosuppressive drugs immunodeficiency

A

inhibit signaling pathways

45
Q

tumors immunodeficiency

A
  • disrupt lymphoid tissue interactions
  • crowd out development of normal immune response
46
Q

aging immunodeficiency

A
  • primarily affects T cells
  • reduced naive T cell production, reduced phagocyte function
  • reduced antibody affinity
47
Q

infection immunodeficiency

A

malaria: inhibits dendritic cell function
measles: infects dendritic cells, decreases T cell responsiveness
staphylococcus: TSS leads to T cell exhaustion
HIV: CD4 depletion

48
Q

immune response to tumors: immunoediting elimination phase

A

elimination phase: neo-antigens recognized, cells attacked and destroyed

49
Q

immune response to tumors: immunoediting equilibrium phase

A
  • lymphocytes and IFN-y put selection pressure on tumor cells that survived elimination to contain tumor
  • results in genetically unstable mutating tumor cells: mutants w/ altered neoantigens
50
Q

immune response to tumors: immunoediting escape phase

A
  • tumor cell variants selected in equilibrium phase can grown in intact environment
  • breach of immune defenses causes resistance to immune detection, tumor expands
51
Q

anti-tumor immunity: NK cells

A
  • respond to stressed/abnormal cells
  • detect and lyse tumor cells w/ no or low MHC 1
  • Have Fc receptors: can kill cells bound to antibody by ADCC
52
Q

anti-tumor immunity: T cells

A
  • mutated antigen must be processed by protease
  • peptide containing mutated AAs bind patient’s MHC I
53
Q

PD-L1, PD-1 inhibition

A

CTL not activated, tumor grows

54
Q

PD-L1, PD-1 blockade

A

CTL activated, tumor killed

55
Q

glucocorticosteroids: target, mechanism

A
  • targets innate and adaptive
  • steroid binds steroid receptor w/ HSP –> can enter nuclear membrane
  • decreases T cell activation, IL-2, neutrophil trafficking, presence of eosinophils, macrophages, DCs
56
Q

cyclosporin: target, mechanism

A
  • targets calcineurin
  • cyclosporin A binds immunophilin, which binds calcineurin instead of calmodulin
  • calcineurin doesn’t activate –> can’t dephosphorylate NFAT
57
Q

rapamycin: target, mechanism

A
  • inhibits AKT/mTOR to decrease T, B cell proliferation and survival
58
Q

cytotoxic drugs: target, mechanism

A
  • inhibit growing cells
  • affects immune system as a whole
  • Low WBCs: patient at risk of infection
59
Q

live attenuated vaccine: advantages

A
  • induces humoral and cell-mediated immunity
  • only one dose needed for long-lasting protection
60
Q

live attenuated vaccine: disadvantages

A
  • pathogen can revert to virulent phenotype
  • transmission from person - person
  • possible adverse rxns
61
Q

live attenuated vaccine: methods

A
  • using closely-related pathogens from different animals
  • growing pathogen in unnatural host/culture
  • administration via unnatural route
  • genetic manipulation
62
Q

inactivated vaccine: methods

A
  • pathogen is killed by exposure to heat, chemicals
63
Q

inactivated vaccine: advantages

A
  • safe: pathogen can’t replicate
  • minimal interference from circulating antibodies
  • easy to make
64
Q

inactivated vaccine: disadvantages

A
  • not as effective as live
  • mostly humoral response, antigens not produced in cells
  • low memory, antigenically weak, contain adjuvants
  • multiple doses needed
65
Q

subunit vaccines: methods

A
  • antigenic fragments of microbes + adjuvants
66
Q

subunit vaccines: advantages

A
  • chemically-defined, can’t replicate: no chance of disease
  • minimal antibody interference
67
Q

subunit vaccines: disadvantages

A
  • not as effective as live, mostly humoral response
  • titer diminishes overtime
  • depends on effective adjuvant
68
Q

autograft

A

self graft

69
Q

isograft

A

identical twin

70
Q

allograft

A

human to human, not identical

71
Q

xenograft

A

different species

72
Q

ABO matching

A
  • lab mixes blood of donor w/ serum of recipient to see if there’s a cross rxn
  • binding donor cells, antibodies from recipient serum
73
Q

hyperacute graft rejection

A
  • from preexisting antibodies
  • occurs within hours
  • IgM to ABO/other antigens
  • IgG against MHC antigens
  • antibodies bind endothelial cells in graft, fix complement
74
Q

acute graft rejection

A
  • days-weeks
  • donor tissue is recognized by immune cells, immune response mounted
  • mostly T cell response, resembling type IV HS
75
Q

acute graft rejection: T cells

A
  • CD8 recognize donor MHC I
  • CD4 recognize donor MHC II
76
Q

acute graft rejection: mechanism

A
  • CD4 T cells activated by graft APCs, leading to inflammation, damage
  • CD8 T cells recognize graft cells, CTL
  • CD4 T recognize graft leading to inflammation, develop alloantibodies
  • alloantibodies bind graft, leading to MAC, ADCC
77
Q

chronic graft rejection

A
  • antibody and T cell mediated
  • loss of graft function
  • months to years later
78
Q

tumor evasion

A
  • lack of T cell recognition of tumor leads to failure to produce tumor antigens, MHC mutations
  • inhibition of T cell activation

Immuno (4 decks)

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