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Micro/Immuno Part 3 > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

Type I hypersensitivity

A
  • immediate
  • mediated by IgE
  • commonly called allergies or atopic disorder
  • atopic individuals are 10-40% of the pop and are genetically susceptible and generally have higher levels of IgE and eosinophils
  • clinical manifestations depend on the route of entry on the antigen and location of the responding cells
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2
Q

common sources of allergens

A
  • inhaled
  • injected
  • ingested
  • contacted
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3
Q

commonalities between allergens

A
  • relatively low MW
  • highly soluble
  • stable proteins carried on particles
  • contain peptides that can be presented by MHC class II
  • effective at activating TH2 cytokines especially IL4 and stimulating and IgE response
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4
Q

require initial sensitization

A
  • antigen activation of TH2 cells and stimulation of IgE class switching in B cells
  • production of IgE
  • binding of IgE to FcRepsilon on mast cell
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5
Q

subsequent exposures

A
  • allergen binds to IgE bound to mast cell
  • releases chemical mediators for immediate ration
  • cytokines cause late phase reaction 2-4 hours later
  • can also cross link IgG, or C5a can bind to complement receptors
  • mast cells also have TLRs-can be turned on in response to LPS
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6
Q

contents of mast cell granules

A
  • histamine
  • TNF
  • tryptase
  • chemokines-CCL3- brings monocytes
  • lipid activators-leukotrienes
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7
Q

two phases

A
  • immediate response is wheal and flare- swelling from leakage and engorgement with RBCs
  • late phase is more widespread swelling and inflammation
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8
Q

effects of mast cell mediators

A

-vascular leakage
-bronchoconstriction
-intestinal hypermobility
^ from amines and lipid mediators
-inflammation-cytokines
-tissue damage-enzymes

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9
Q

SRS-A

A
  • slow releases substance of anaphylaxis

- mixture of leukotrienes produced during response

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10
Q

serotonin

A

vascular perm

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11
Q

TNF

A

expression of adhesion molecules on endothelial cells

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12
Q

mediators bring in

A
  • IF cells
  • basophils
  • eosinophils
  • reciprocally regulated- TGFb and IL3 increase basophils and decrease eosinophils
  • IL5 and GM-CSF increase eosinophils
  • usually low levels until activated, then can expresses IgE FcR
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13
Q

granulocytes and parasites

A
  • promotes expulsion of parasites by increased peristalsis and mucous
  • kills parasites and host cells and helps with tissue remodeling
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14
Q

responses to subQ allergen

A
  • insect saliva
  • low dose
  • activates mast cells
  • increase vascular perm and localized swelling
  • urticaria is localized, deeper more diffuse swelling is angiodema
  • mechanism in skin testing for allergies (RAST assay for allergen specific IgE)
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15
Q

responses to inhaled allergen

A
  • allergic rhinitis
  • antigen taken in by APC activates TH2 cells which make IgE first time via IL4
  • second time inhaled and antigen activates local mucosal mast cells
  • causes blood vessel perm and activation of epithelium
  • eosinophils recruited (IL5 and GM-CSF) and enters nasal passages with mucous
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16
Q

allergic asthma

A
  • acute-mucosal mast cell captures antigen
  • IF mediators contract smooth muscle, increase mucous secretion from airway epithelium and increase BV perm

chronic

  • mediated by cytokines and eosinophil products
  • can occur in absence of allergen- other irritants like cold or smoke
  • leads to tissue remodeling and mucous plugs

TH2 cells-IL13?

17
Q

reactions to adsorbed antigen

A
  • food
  • ingestion activates mucosal mast cells in gut
  • release histamine, which acts on epithelium, BV, and smooth muscle
  • antigen diffuses into blood vessels and is widely distributed causing urticaria
  • smooth muscle contraction is vomiting and diarrhea
  • fluid flows into gut lumen
18
Q

responses to systemic allergin

A
  • systemic anaphylaxis
  • drugs, serum, venom, peanuts
  • epipen-tight junctions, relaxes smooth muscle, activates heart
  • antigen in bloodstream enters tissues and activates CT mast cells throughout the body
  • mast cells degranulate and release IF mediators
  • drop in BP is fatal
  • contracts airway
  • cramps and vomiting
19
Q

genetic predisposition

A
  • MHC and non MHC
  • TcR
  • IL4
  • IL4R
  • IgE Receptor
  • structural variants
  • increases the immune response
20
Q

hypersensitivity doubled

A

-hygiene and low parasites

21
Q

hygiene hypothesis

A
  • poorer hygiene results in exposure to Tg1 inducing infections which protect against allergy
  • little allergy seen in worm infections in developing countries that need TH2?
22
Q

counter regulation hypothesis

A
  • infections lead to production of IL10 and TGFb which downregulates TH1 and TH2
  • less hypersensitivity
  • clean and genetic=allergies
23
Q

treatment for type I sensitivity

A
  • avoid the allergen
  • treat symptoms with antihistamines, corticosteroids, singulair, epi, albuterol
  • desensitization-controlled exposure to increased dose of antigen over time leads to IgA and G antibodies which block binding of allergen to IgE
  • allergenic peptide vaccination to anergize allergen specifiv T cells
  • anti IgE
  • block effectors-anti cytokines
24
Q

Type II, III, IV

A
  • may occur in response to foreign antigen
  • also when an individuals immune system reacts against autologous or modulated self antigens
  • impacted by genetic susceptibility and environmental factors
25
Q

Type II

A
  • antibodies bind to a cell associated antigen or cell surface receptor and fix antigen
  • penicillin modifies proteins on RBCs and IgG binds to it
  • leads to lysis or complement and phago
  • when platelets its thrombocytopenia
  • significant in ABO transfusions- we have antiA, B or both
26
Q

Type III

A
  • large quantities of soluble antigens and their antibodies develop and form large latticed immune complexes
  • isotype, valency, charge, and ability to fix complement determine IC pathogenicity
  • latticed immune complexes are pathologically capable of depositing systemically in any of a variety of tissue sites, creating downstream cellular damage with many different clinical presentations
  • serum sickness
  • kidney problems
27
Q

arthus reaction

A
  • locally injected antigen in immune individual with IgG
  • local immune complex formation activates complement, C5a binds to a receptor on mast cell
  • the antibody complex also binds to the mast cell and induces degranulation
  • local IF, increased fluid and protein release, phago, blood vessel occlusion
  • PMNs attracted and produce lysosomal enzymes
  • tetanus booster at less than 5 years
28
Q

serum sickness

A
  • occurs after the development of antibody, 7-10 days
  • may occur after large amounts of foreign protein such as antisera for snake bite, mouse antibodies, streptokinase
  • second time can happen 1-3 days
29
Q

type IV

A
  • delayed type from proteins leading to local skin swelling
  • contact type from poison ivy leading to local epidermal reaction
  • gluten sensitive-atrophy in small bowel and malabsorption
  • TH1 cells important-chemokines, IFN gamma, TNFa and LT, IL3 and GM-CSF
30
Q

delayed type sensitivity

A
  • antigen introduced subQ and processed by APCs
  • TH1 recognizes and releases cytokines
  • T cells, phago, fluid and protein to site
  • PPD
31
Q

contact hypersensitivity

A
  • CD4 cells activate other immune cells while CD8 cells kill chemical reacted cells that display foreign antigen
  • poison ivy toxin modifies our skin protein
  • first time ok, second time lots of active T cells
32
Q

treatment of type 2,3,4

A
  • avoid antigen
  • reduce the impact of the immune response with antiinflammatories, steroids
  • reduce immune response in general (steroids) or specifically (target B and T cells)
  • induce regulation of the response (Treg)
  • block the effector mechanisms of allergic response cytokines, co stim molecules
33
Q

Type IV

A

TH1 cells

chemokines, IFN gamma, TNFa and LT, IL3 and GM-CSF

Micro/Immuno Part 3 (12 decks)

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