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Microbiology/Immunology > hypersensitivity reactions > Flashcards

hypersensitivity reactions Flashcards

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1
Q

which type of hypersensitivity reaction does not involve antibodies

A

type IV or delayed type hypersensitivity

aka T cell mediated

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2
Q

how is type I reaction mediated

A

antigen binds to surface of IgE coated basophils or mast cells

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3
Q

is type I reaction a TH1 or TH2 mediated response

A 
TH2 mediated (IgE)
because allergens enter in absence of inflammation, and TH2 response occurs in absence of inflammation
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4
Q

meaning of atopic

A

individual with increased tendency to develop type I hypersensitivity
due to increased production of IL-4 –> increased production of IgE, as well as having receptors with greater affinity for IgE

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5
Q

why does type I occur at skin, lungs, and gut

A

this is where basophils and mast cells exist, where body produces IgE

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6
Q

hygiene hypothesis

A

decreased exposure to pathogens during childhood –> decreased TH1 response –> bigger TH2 response resulting in increased IgE production

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7
Q

basophil characteristics

A 
non-phagocytotic
purple granules
<1% peripheral blood WBCs
related to mast cells
prominent role in allergies
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8
Q

can anaphylaxis occur on first exposure

A

no, only activate B cells, form plasma cells, and then form IgE on first exposure

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9
Q

what does IgE bind on first exposure in type I reaction

A

Fc receptors on basophils and mast cells

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10
Q

on 2nd or 3rd exposure in type I reaction, what happens

A

CROSS-LINKING of IgE:
allergen binds surface bound IgE and basophils/mast cells release granules (histamine)
histamine causes increased vascular permeability and smooth muscle contraction

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11
Q

effects of histamine

A

increased vascular permeability and smooth muscle contraction

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12
Q

what causes release of histamine granules

A

cross-linking of IgE: allergen binding to surface IgE on basophils and mast cells

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13
Q

what does cross-linking of IgE result in

A

degranulation of basophils and mast cells (release of histamine)

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14
Q

why must anaphylactic patients be monitored after initial treatment

A

potential late phase response

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15
Q

mast cell granules contents other than histamine

A

TNF alpha (promotes inflammation)
proteases (cause tissue damage)
eosinophil chemotactic factor of anaphylaxis (attracts eosinophils)

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16
Q

how are leukotrienes different from histamine

A

must be synthesized (not already made in granules), therefore released more slowly
longer effect

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17
Q

effects of leukotrienes

A

increased vascular permeability
smooth muscle contraction
(same as histamine)

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18
Q

when do leukotrienes come into play

A

late phase reaction

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19
Q

characteristics of eosinophils

A

non-phagocytotic
orange granules
anti-parasite immunity and allergy
attach to worms and release hydrolytic enzymes to kill parasite

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20
Q

what substances are involved in late phase response of type I reaction

A

PGs, leukotrienes, chemokines, and cytokines secreted by mast cells

21
Q

only treatment that reverses anaphylaxis

A

epinephrine

22
Q

effect of antihistamines

A

binds histamine receptors, blocking binding of histamine

23
Q

what treatments block degranulation of basophils and mast cells

A

cromolyn sodium

theophylline

24
Q

what treatment binds histamine receptors

A

antihistamines

25
Q

effect of epinephrine

A 
binds beta adrenergic receptors
increases cAMP
relaxation of bronchial smooth muscle
tightening of endothelial junctions
stimulation of heart
26
Q

what are 2 treatments for highly allergic patients

A

repeated subcutaneous allergen injections

humanized mouse anti-IgE antibody

27
Q

how does humanized mouse anti-IgE antibody treatment work

A

humanized mouse antibody binds IgE to prevent binding to IgE receptors
95% reduction in serum IgE and downregulation of Fc receptors

28
Q

how does repeated subq allergen injection affect antibodies

A

IgE levels decrease
IgG levels increase
mechanism unknown

29
Q

what type of hypersensitivity is antibody-mediated cytotoxicity

A

type II

30
Q

mechanism of type II

A

cell destruction mediated by reaction of antibody to cell surface bound antigen
either opsonization and phagocytosis OR classical complement pathway

31
Q

hemolytic disease of newborn is an example of what type of hypersensitivity

A

type II reaction (antibody-mediated cytotoxicity)

32
Q

two examples of type II non-cytotoxic reaction with cell receptors

A

Grave’s disease

myasthenia gravis

33
Q

mechanism of Grave’s

A

antibodies to TSH receptor causes overproduction of thyroid hormones –> hyperthyroidism

34
Q

mechanism of myasthenia gravis

A

antibodies to ACh receptors block nerve impulse transmission to muscles

35
Q

mechanism of ADCC in type II

A

tumor or virus infected cells are bound by IgG and are lysed by NK cells, monocytes, or neutrophils via recognition through Fc receptors

36
Q

mechanism of type II complement-mediated reactions

A

complement activation by IgG or IgM

cell lysis OR opsonization –> phagocytosis

37
Q

examples of type II reactions

A 
transfusion reactions
autoimmune hemolytic anemia
drug reactions
hemolytic disease of newborn
grave's
myasthenia gravis
38
Q

what type of hypersensitivity involves immune complexes

A

type III

39
Q

what are 4 ways that immune complex disease can be induced

A 
autoimmune disease (SLE, RA)
drug reactions (penicillin, sulphonamides)
infectious disease (bacterial endocarditis, chronic viral hepatitis, post-streptococcal glomerulonephritis)
inhaled allergens (farmer's lung)
40
Q

pathogenesis of type III reaction

A

exposure to antigen –> formation of ABs that can react with antigen to form immune complexes
complexes lodge in tissues
complement activated –> inflammatory reaction
lysosomal enzymes released to try to remove complexes –> cause damage to healthy tissue –> fever, urticaria, arthritis, etc.

41
Q

examples of type III reaction

A 
SLE
RA
serum sickness
bacterial endocarditis
post-streptococcal glomerulonephritis
chronic viral hepatitis
farmer's lung
42
Q

what normally happens to immune complexes in healthy patients

A

RBCs bear CR1 protein that binds C3b and C4b on immune complexes
complexes are shuttled to liver and spleen via RBCs
in liver and spleen, complexes are removed from RBCs and degraded by macrophages
when system is overwhelmed, disease develops

43
Q

which hypersensitivity is delayed type

A

type IV (cell-mediated)

44
Q

which type of hypersensitivity does NOT involve antibodies

A

type IV delayed type/cell-mediated

45
Q

when does type IV reaction manifest

A

24-72 hours after exposure to antigen

46
Q

examples of type IV hypersensitivity

A

TB skin test reaction
contact dermatitis
delayed graft reaction

47
Q

mechanism of contact dermatitis (type IV reaction)

A 
haptens complex with skin proteins and are internalized
expressed on cell surface of APCs on class I MHC
activate CTLs --> secrete inflammatory cytokines
48
Q

mechanism of TB skin test (type IV reaction)

A

macrophages cause damage
macrophages present antigen on class II MHC to antigen-specific memory T cells
T cells secrete IFN gamma –> activates macrophages –> amplification

Microbiology/Immunology (30 decks)

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