Karteikarten
Hypersensitivity and Allergy
Karten in diesem Stapel (15)
- 1What is hypersensitivity?Immune responses which are damaging rather than helpful to the host
- 2Distinguish between the 4 types (that we covered in lectures) of hypersensitivity (duration, mediated by_ & disease examples)
- 3Type 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) - 4What the primary and secondary mediators?primary: histamines, serotonin and tryptase
secondary: leukotrienes, prostaglandins, bradykinin and heparin - 5what 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) - 6Type 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 - 7Initial and late type I response to allergeninitial: vasodilation, vascular leakage, smooth muscle spasm
late: mucosal edema & secretion, leukocyte infiltration, epithelial damage and bronchospasm - 8what is anaphylaxiswhen inflammation in response to an allergen becomes systemic
- 9ways 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 - 10What 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 - 11what 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 - 12what 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 - 13mechanism 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) - 14type 4- Malfunction in immune system recognition ability
-processing of antigen in contact with skin (can be seen in the gut as well) - 15What are the types imptt to allergy - and summarize main pointsType 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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- Beschreibung
- university Infection, Immune and Immunology Karteikarten am Hypersensitivity and Allergy, erstellt von Aline Mola am 15/12/2014.
- Erstellt von
- Aline Mola
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- 60
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