Type II hypersensitivity
| Type II hypersensitivity | |
|---|---|
| Video explanation | |
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| Specialty | Immunology |
Type II hypersensitivity, in the Gell and Coombs classification of allergic reactions, is an antibody mediated process in which IgG and IgM antibodies are directed against antigens on cells (such as circulating red blood cells) or extracellular material (such as basement membrane). This subsequently leads to cell lysis, tissue damage or loss of function through mechanisms such as
- complement activation via the classical complement pathway
- antibody dependent cell-mediated cytotoxicity or
- anti-receptor activity.[1]
The activation of the complement system results in opsonization, the agglutination of red blood cells, cell lysis, and cell death.[2]
These reactions usually take between 2 and 24 hours to develop.[2]
Examples
| Disease | Autoantibody target |
|---|---|
| Autoimmune hemolytic anemia | Red blood cells |
| Goodpasture syndrome | Glomerular basement membrane |
| Graves disease | Thyroid stimulating hormone receptor |
| Immune thrombocytopenia | Platelets |
| Myasthenia gravis | Muscle acetylcholine receptor |
An example of complement dependent type II hypersensitivity is an acute haemolytic transfusion reaction following transfusion of ABO incompatible blood.[4] Preformed antibody (predominantly IgM) against donor red cell antigens not found in an individual of a particular blood group (e.g. anti-A IgM in an individual with blood group B), bind to the donor red cell surface and lead to rapid complement mediated haemolysis and potentially life-threatening clinical consequences.
Another example of a complement dependent type II hypersensitivity reaction is Goodpasture's syndrome, where the basement membrane (containing collagen type IV) in the lung and kidney is attacked by one's own antibodies in a complement mediated fashion.[5]
An example of anti-receptor type II hypersensitivity (also classified as type V hypersensitivity) is observed in Graves disease, in which anti-thyroid stimulating hormone receptor antibodies lead to increased production of thyroxine.[6]
However, there are questions as to the relevance of the Gell and Coombs classification of allergic reactions in modern-day understanding of allergy and it has limited utility in clinical practice.[7]
See also
References
- ↑ "Immunopathology". Archived from the original on 1 September 2017. Retrieved 17 March 2019.
- ↑ 2.0 2.1 Warrington, Richard; Watson, Wade; Kim, Harold L.; Antonetti, Francesca Romana (10 November 2011). "An introduction to immunology and immunopathology". Allergy, Asthma, and Clinical Immunology. 7 (1): S1. doi:10.1186/1710-1492-7-S1-S1. ISSN 1710-1492. PMC 3245432. PMID 22165815.
- ↑ "Hypersensitivity reactions". Amboss. Archived from the original on 20 April 2019. Retrieved 20 April 2019.
- ↑ Tinegate, Hazel; Birchall, Janet; Gray, Alexandra; Haggas, Richard; Massey, Edwin; Norfolk, Derek; Pinchon, Deborah; Sewell, Carrock; Wells, Angus; Allard, Shubha (October 2012). "Guideline on the investigation and management of acute transfusion reactions Prepared by the BCSH Blood Transfusion Task Force". British Journal of Haematology. 159 (2): 143–153. doi:10.1111/bjh.12017. PMID 22928769.
- ↑ Goodpasture Syndrome at eMedicine
- ↑ Graves Disease at eMedicine
- ↑ Descotes, Jacques; Choquet-Kastylevsky, Geneviève (February 2001). "Gell and Coombs's classification: is it still valid?". Toxicology. 158 (1–2): 43–49. doi:10.1016/S0300-483X(00)00400-5.
External links
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| External resources |