hypersensitivity reactions Flashcards by Emily Nelson

which type of hypersensitivity reaction does not involve antibodies

type IV or delayed type hypersensitivity

aka T cell mediated

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how is type I reaction mediated

antigen binds to surface of IgE coated basophils or mast cells

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is type I reaction a TH1 or TH2 mediated response

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

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meaning of atopic

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

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

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hygiene hypothesis

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

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basophil characteristics

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

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can anaphylaxis occur on first exposure

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

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what does IgE bind on first exposure in type I reaction

Fc receptors on basophils and mast cells

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

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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effects of histamine

increased vascular permeability and smooth muscle contraction

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what causes release of histamine granules

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

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what does cross-linking of IgE result in

degranulation of basophils and mast cells (release of histamine)

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why must anaphylactic patients be monitored after initial treatment

potential late phase response

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mast cell granules contents other than histamine

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

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how are leukotrienes different from histamine

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

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effects of leukotrienes

increased vascular permeability
smooth muscle contraction
(same as histamine)

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when do leukotrienes come into play

late phase reaction

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characteristics of eosinophils

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

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

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

only treatment that reverses anaphylaxis

epinephrine

effect of antihistamines

binds histamine receptors, blocking binding of histamine

what treatments block degranulation of basophils and mast cells

cromolyn sodium

theophylline

what treatment binds histamine receptors

antihistamines

effect of epinephrine

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

what are 2 treatments for highly allergic patients

repeated subcutaneous allergen injections | humanized mouse anti-IgE antibody

how does humanized mouse anti-IgE antibody treatment work

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

how does repeated subq allergen injection affect antibodies

IgE levels decrease IgG levels increase mechanism unknown

what type of hypersensitivity is antibody-mediated cytotoxicity

type II

mechanism of type II

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

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

type II reaction (antibody-mediated cytotoxicity)

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

Grave's disease | myasthenia gravis

mechanism of Grave's

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

mechanism of myasthenia gravis

antibodies to ACh receptors block nerve impulse transmission to muscles

mechanism of ADCC in type II

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

mechanism of type II complement-mediated reactions

complement activation by IgG or IgM | cell lysis OR opsonization --> phagocytosis

examples of type II reactions

``` transfusion reactions autoimmune hemolytic anemia drug reactions hemolytic disease of newborn grave's myasthenia gravis ```

what type of hypersensitivity involves immune complexes

type III

what are 4 ways that immune complex disease can be induced

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

pathogenesis of type III reaction

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.

examples of type III reaction

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

what normally happens to immune complexes in healthy patients

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

which hypersensitivity is delayed type

type IV (cell-mediated)

which type of hypersensitivity does NOT involve antibodies

type IV delayed type/cell-mediated

when does type IV reaction manifest

24-72 hours after exposure to antigen

examples of type IV hypersensitivity

TB skin test reaction contact dermatitis delayed graft reaction

mechanism of contact dermatitis (type IV reaction)

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

mechanism of TB skin test (type IV reaction)

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