Hypersensitivity and Allergy

Aline Mola
Flashcards by Aline Mola, updated more than 1 year ago
Aline Mola
Created by Aline Mola about 5 years ago


university Infection, Immune and Immunology Flashcards on Hypersensitivity and Allergy, created by Aline Mola on 12/15/2014.

Resource summary

Question Answer
What is hypersensitivity? Immune responses which are damaging rather than helpful to the host
Distinguish between the 4 types (that we covered in lectures) of hypersensitivity (duration, mediated by_ & disease examples) Screen_Shot_2014-12-15_at_23.52.30.png (image/png)
Type I hypersensitivity: what is the malfunction of IgE - mast cell response? -bone marrow IgE makes specific antigen that leaves & binds to mast cells via IgE-FC receptors, which activates the mast cell -leads to mass degranulation and thus localised inflammation -Mast cells have vesicles of pro-inflammatory mediators (histamine and proteases - tryptase)
What the primary and secondary mediators? primary: histamines, serotonin and tryptase secondary: leukotrienes, prostaglandins, bradykinin and heparin
what does degranulation of mast cells lead to and which mediator causes it? - vascular permeability (by histamines, leukotrienes and bradykinin) - smooth muscle contraction (by serotonin) - bronchoconstriction (by prostaglandins) - mucus production (by bradykinin) - anti-coagulant (by heparin)
Type I response to allergen - Antigen (allergen) detected by IgE B cell, which produces antibodies that bind to mast cell's IgE Fc receptors which release mediators - allergen also binds to TCR which recruits eosinophils which activate granule release
Initial and late type I response to allergen initial: vasodilation, vascular leakage, smooth muscle spasm late: mucosal edema & secretion, leukocyte infiltration, epithelial damage and bronchospasm
what is anaphylaxis when inflammation in response to an allergen becomes systemic
ways of diagnosing type I hypersensitivity - Measure mast cell tryptase levels in serum - indicates mast cell degranulation (problem: tryptase breaks down fast, also should be cleared in 6h) - clinical history of symptoms - skin prick test (good but can't do it if pregnany, histor of anaphylaxis, etc) - if cant do skin prick - ImmunoCap to detect allergen-specific IgE levels
What is type 2 hypersensitivity - Malfunction immune system activation via Ig binding - Usually seen in Ig binding to bact. - leads to opsonisation and activates complement and innate cells - Ultimately leads to death of cell layer
what is the mechanism of Type 2 hypersensitivity? - Binding of autoreactive Ig (autoantibody), to its target antigen in host cell bound protein -leads to activation of complement and innate cells (neutrophils & macrophages) - Leads to breakdown and death of host cell
what was the type 3 hypersensitivity originally designed for and when is it problematic? - Originally to clear away soluble foreign antigen bound to Ig - if there is large amounts of Ig and respective antigen in one area can lead to an exaggerated response eg.: rheumatoid arthritis
mechanism of type 3 hypersensitivity -more immune complex formed but not enough complement supply or cells to interact with - increases deposition of immune complex on the walls of blood vessels - Immune activation now directed against the vessel -> degradation of vessel walls (vasculitis)
type 4 - Malfunction in immune system recognition ability -processing of antigen in contact with skin (can be seen in the gut as well)
What are the types imptt to allergy - and summarize main points Type 1: fast response - by binding of allergen to IgE bound to mast cells leadig to mast cell degranulation = localised inflammation. diagnosed by clinical history, skin prick tests and specific IgE tests Type 4 – delayed type reaction, involves T-cells and leads to contact dermatitis. diagnosed by clinical history and patch tests
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