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Flashcards in Hypersensitivity Deck (19)
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describe type I hypersensitivity

  • sensitization
    • antigen contact, typically low-dose via mucous membranes (respiratory, GI), IgE production
  • elicitation (re-exposure)
    • pre-formed IgE (allergen-specific) triggers mast cell activation mediator release
  • reactions
    • can occur within seconds-minutes of exposure
  • severity ranges from irritating to fatal


describe the sensitization response

  • IgE produced by plasma cells is rapidly taken up by FcER1 on tissue mast cells and circulating basophils (serum 2 days; compare to IgG, which is 21 days)


describe the early phase of the sensitization response

  • IgE crosslinking by antigen release of preformed mediators
    • immedate release of histamine
      • smooth muscle constriction, vasodilation, vascular leak, GI motility (increased), mucous secretion, sensory nerve activation
  • followed by rapid production of arachidonic acid products
    • within minutes: leukotrienes, prostaglandins


describe the late phase of the sensitization response

  • gene activation leads to new cytokine production ~6 hours after antigen triggering
    • TNFa
      • recruit inflammatory cells
    • IL-3, IL-5, GM-CSF
      • eosinophil production
    • IL-4, IL-13
      • propogate Th2 response


the innate responder cell in type I hypersensitivtiy is ____

describe this

the innate responder cell in type I hypersensitivtiy is eosinophils

  • production of eosinophils in bone marrow driven by: IL-5 (Th2 cytokine); also IL-3 and GM-CSF
  • chemotaxis from blood to tissue sites utilizes:
    • IL-5
    • eotaxins (CCL11, CCL24, CCL26)
  • primed for activation by IL-5, eotaxins C3a/C5a
  • expression of FcR for IgG, IgA, IgE 


the most potent trigger for eosinophils is ____

what does it release?

the most potent trigger for eosinophils is FcR-crosslinking

  • results in exocytosis of preformed toxic proteins
    • major basic protein
    • eosinophil cationic protein
    • eosinophil-derived neurotoxin
  • propagate the response:
    • secrete IL-3, IL-5, GM-CSF
    • secrete IL-8 (PMN attractant)


describe the manifestations of Type I Hypersensitivity

  • respiratory mucosa
    • allergic
    • rhinitis
    • asthma
  • GI mucosa
    • food allergy
  • skin
    • contact urticaria
  • circulation
    • anaphylaxis


describe the process of anaphylaxis

  • response to systemic circulation of allergen
  • IgE cross-linking on mast cells in perivascular tissue
  • circulating histamine, PGs/LTs --> vasodilation, vascular leak
  • high-output shock: decreased BP despite increased CO


in Type II (cytotoxic) Hypersensitivity, the damaged is mediated by _____

in type II hypersensitivity, the damage is mediated by tissue-specific IgG or IgM


describe the hapten response

  • mechanism of sensitization
    • a foreign agent (typically drug) acts as a hapten
    • conjugates self protein modified self
    • T cell/B cell response high affinity
    • anti-self IgG or IgM
  • on re-exposure
    • hapten conjugation to self modified
    • binding of IgG or IgM to modified self tissue (platelet, RBC) 
    • activation of normal immunoglobulin effector


summarize the antibody function and then the resulting syndrome 


describe type III (immune complex) hypersensitivity


describe type IV (delayed) hypersensitivity

  • group of T cell mediated responses to antigen
    • direct killing of target cells (by CD8 T cells)
    • indirect via activation of macrophages (CD4 T cells)
    • sensitization is required
    • on re-exposure: reactions occur over 1-3 days
    • T cells are necessary and sufficient


____ do not have type IV reactions

athymic subjects do not have type IV reactions


describe the pathogenesis of type IV hypersensitivity


summarize hypersensitivity type I


summarize type II hypersensitivity


summarize type III hypersensitivities


summarize type IV hypersensitivities