Autoimmune hemolytic anemia pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
===Warm autoimmune hemolytic anemia=== | ===Warm autoimmune hemolytic anemia=== | ||
The pathophysiology of warm autoimmune hemolytic anemia involves immunoglobulin G (IgG) antibodies binding to [[red blood cells]] at a temperature of 37 degrees Celcius. <ref name="pmid15637139">{{cite journal| author=Mqadmi A, Zheng X, Yazdanbakhsh K| title=CD4+CD25+ regulatory T cells control induction of autoimmune hemolytic anemia. | journal=Blood | year= 2005 | volume= 105 | issue= 9 | pages= 3746-8 | pmid=15637139 | doi=10.1182/blood-2004-12-4692 | pmc=1895013 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15637139 }} </ref> The designation of ''warm'' is based on the fact the optimal binding temperature is 37 degrees Celcius, or normal body temperature. Macrophages bind to the antibody-coated [[red blood cells]] via the Fc receptors and result in extravascular destruction. | The pathophysiology of warm autoimmune hemolytic anemia involves immunoglobulin G (IgG) antibodies binding to [[red blood cells]] at a temperature of 37 degrees Celcius. <ref name="pmid15637139">{{cite journal| author=Mqadmi A, Zheng X, Yazdanbakhsh K| title=CD4+CD25+ regulatory T cells control induction of autoimmune hemolytic anemia. | journal=Blood | year= 2005 | volume= 105 | issue= 9 | pages= 3746-8 | pmid=15637139 | doi=10.1182/blood-2004-12-4692 | pmc=1895013 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15637139 }} </ref> The designation of ''warm'' is based on the fact the optimal binding temperature is 37 degrees Celcius, or normal body temperature. Macrophages bind to the antibody-coated [[red blood cells]] via the Fc receptors and result in extravascular destruction. It has been shown that induction of autoimmune hemolytic anemia is controlled by an immunosuppressive population of T lymphocytes known as [[regulatory T cells]]. | ||
==References== | ==References== | ||
Revision as of 22:23, 16 March 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Assosciate Editor(s)-In-Chief: Prashanth Saddala M.B.B.S; Shyam Patel [2]
Overview
Pathophysiology
Warm autoimmune hemolytic anemia
The pathophysiology of warm autoimmune hemolytic anemia involves immunoglobulin G (IgG) antibodies binding to red blood cells at a temperature of 37 degrees Celcius. [1] The designation of warm is based on the fact the optimal binding temperature is 37 degrees Celcius, or normal body temperature. Macrophages bind to the antibody-coated red blood cells via the Fc receptors and result in extravascular destruction. It has been shown that induction of autoimmune hemolytic anemia is controlled by an immunosuppressive population of T lymphocytes known as regulatory T cells.
References
- ↑ Mqadmi A, Zheng X, Yazdanbakhsh K (2005). "CD4+CD25+ regulatory T cells control induction of autoimmune hemolytic anemia". Blood. 105 (9): 3746–8. doi:10.1182/blood-2004-12-4692. PMC 1895013. PMID 15637139.