Myasthenia gravis causes: Difference between revisions
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# [[MHC|The Major Histocompatibility Complex]]: In genetic etiology of most of the [[autoimmune diseases]] including [[Myasthenia gravis|MG]], [[MHC]] genes play the most important role.<ref name="pmid4544224">{{cite journal |vauthors=Feltkamp TE, van den Berg-Loonen PM, Nijenhuis LE, Engelfriet CP, van Rossum AL, van Loghem JJ, Oosterhuis HJ |title=Myasthenia gravis, autoantibodies, and HL-A antigens |journal=Br Med J |volume=1 |issue=5899 |pages=131–3 |date=January 1974 |pmid=4544224 |pmc=1633001 |doi= |url=}}</ref> | # [[MHC|The Major Histocompatibility Complex]]: In genetic etiology of most of the [[autoimmune diseases]] including [[Myasthenia gravis|MG]], [[MHC]] genes play the most important role.<ref name="pmid4544224">{{cite journal |vauthors=Feltkamp TE, van den Berg-Loonen PM, Nijenhuis LE, Engelfriet CP, van Rossum AL, van Loghem JJ, Oosterhuis HJ |title=Myasthenia gravis, autoantibodies, and HL-A antigens |journal=Br Med J |volume=1 |issue=5899 |pages=131–3 |date=January 1974 |pmid=4544224 |pmc=1633001 |doi= |url=}}</ref> | ||
# The [[CHRNA1]] [[Locus]]: The [[Translation (genetics)|translation]] product of this [[gene]] is the alpha subunit of [[Acetylcholine receptor|AChR]], which is the target of many [[autoantibodies]] in myasthenia gravis patients.<ref name="pmid9700504">{{cite journal |vauthors=Tzartos SJ, Barkas T, Cung MT, Mamalaki A, Marraud M, Orlewski P, Papanastasiou D, Sakarellos C, Sakarellos-Daitsiotis M, Tsantili P, Tsikaris V |title=Anatomy of the antigenic structure of a large membrane autoantigen, the muscle-type nicotinic acetylcholine receptor |journal=Immunol. Rev. |volume=163 |issue= |pages=89–120 |date=June 1998 |pmid=9700504 |doi= |url=}}</ref> | # The [[CHRNA1]] [[Locus]]: The [[Translation (genetics)|translation]] product of this [[gene]] is the alpha subunit of [[Acetylcholine receptor|AChR]], which is the target of many [[autoantibodies]] in myasthenia gravis patients.<ref name="pmid9700504">{{cite journal |vauthors=Tzartos SJ, Barkas T, Cung MT, Mamalaki A, Marraud M, Orlewski P, Papanastasiou D, Sakarellos C, Sakarellos-Daitsiotis M, Tsantili P, Tsikaris V |title=Anatomy of the antigenic structure of a large membrane autoantigen, the muscle-type nicotinic acetylcholine receptor |journal=Immunol. Rev. |volume=163 |issue= |pages=89–120 |date=June 1998 |pmid=9700504 |doi= |url=}}</ref> | ||
# The [[PTPN22]] [[Gene]]: | # The [[PTPN22]] [[Gene]]: This [[gene]] is responsible for producing an intracellular protein phosphatase [[PTPN22]]. The impaired binding of this protein to protein tyrosine kinase Csk occurs as a result of a missense polymorphism which replace [[arginine]] with [[tryptophan]]. Activity of [[PTPN22]] will increase and inhibits [[T cell]] activation and [[interleukin 2]] production which leads to predisposition to [[autoimmunity]]. | ||
# The [[FCGR2A|FCGR2]] [[Locus]]: | # The [[FCGR2A|FCGR2]] [[Locus]]: | ||
# The [[CTLA-4|CTLA4]] [[Locus]]: | # The [[CTLA-4|CTLA4]] [[Locus]]: | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Causes
Myasthenia gravis may be caused by:
- Thymus abnormalities:
Thymus abnormalities including thymic hyperplasia and thymoma are very common in myasthenia gravis and thymectomy is one of the treatment of this disease.[1][2] In thymus, we have myoid cells which present intact AChR on their surface. On the other hand thymic epithelial cells produce AChR subunits which activate helper T cells. These T cells attack AChR on the myoid cells and the cascade of antibody production and complement activation will begin.[3][4][5]
- Genetic:
- The Major Histocompatibility Complex: In genetic etiology of most of the autoimmune diseases including MG, MHC genes play the most important role.[6]
- The CHRNA1 Locus: The translation product of this gene is the alpha subunit of AChR, which is the target of many autoantibodies in myasthenia gravis patients.[7]
- The PTPN22 Gene: This gene is responsible for producing an intracellular protein phosphatase PTPN22. The impaired binding of this protein to protein tyrosine kinase Csk occurs as a result of a missense polymorphism which replace arginine with tryptophan. Activity of PTPN22 will increase and inhibits T cell activation and interleukin 2 production which leads to predisposition to autoimmunity.
- The FCGR2 Locus:
- The CTLA4 Locus:
- environment:
- Drugs:
- Infections:
- Trauma:
References
- ↑ Drachman DB (June 1994). "Myasthenia gravis". N. Engl. J. Med. 330 (25): 1797–810. doi:10.1056/NEJM199406233302507. PMID 8190158.
- ↑ Vincent A (October 2002). "Unravelling the pathogenesis of myasthenia gravis". Nat. Rev. Immunol. 2 (10): 797–804. doi:10.1038/nri916. PMID 12360217.
- ↑ Willcox N, Leite MI, Kadota Y, Jones M, Meager A, Subrahmanyam P, Dasgupta B, Morgan BP, Vincent A (2008). "Autoimmunizing mechanisms in thymoma and thymus". Ann. N. Y. Acad. Sci. 1132: 163–73. doi:10.1196/annals.1405.021. PMID 18567866.
- ↑ Leite MI, Jones M, Ströbel P, Marx A, Gold R, Niks E, Verschuuren JJ, Berrih-Aknin S, Scaravilli F, Canelhas A, Morgan BP, Vincent A, Willcox N (September 2007). "Myasthenia gravis thymus: complement vulnerability of epithelial and myoid cells, complement attack on them, and correlations with autoantibody status". Am. J. Pathol. 171 (3): 893–905. doi:10.2353/ajpath.2007.070240. PMC 1959483. PMID 17675582.
- ↑ Hohlfeld R, Wekerle H (September 2008). "Reflections on the "intrathymic pathogenesis" of myasthenia gravis". J. Neuroimmunol. 201-202: 21–7. doi:10.1016/j.jneuroim.2008.05.020. PMID 18644632.
- ↑ Feltkamp TE, van den Berg-Loonen PM, Nijenhuis LE, Engelfriet CP, van Rossum AL, van Loghem JJ, Oosterhuis HJ (January 1974). "Myasthenia gravis, autoantibodies, and HL-A antigens". Br Med J. 1 (5899): 131–3. PMC 1633001. PMID 4544224.
- ↑ Tzartos SJ, Barkas T, Cung MT, Mamalaki A, Marraud M, Orlewski P, Papanastasiou D, Sakarellos C, Sakarellos-Daitsiotis M, Tsantili P, Tsikaris V (June 1998). "Anatomy of the antigenic structure of a large membrane autoantigen, the muscle-type nicotinic acetylcholine receptor". Immunol. Rev. 163: 89–120. PMID 9700504.