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===Autoimmune disease=== ====Autoimmune polyendocrine syndrome==== [[Autoimmune polyendocrine syndrome type 1]] is a rare genetic autoimmune syndrome that results from a genetic defect of the thymus tissues.{{sfn|Harrison's|2015|pp=2756-7}} Specifically, the disease results from defects in the [[autoimmune regulator]] (AIRE) gene, which stimulates expression of self antigens in the epithelial cells within the medulla of the thymus. Because of defects in this condition, self antigens are not expressed, resulting in T cells that are not conditioned to tolerate tissues of the body, and may treat them as foreign, stimulating an immune response and resulting in autoimmunity.{{sfn|Harrison's|2015|pp=2756-7}} People with APECED develop an autoimmune disease that affects multiple [[endocrine]] tissues, with the commonly affected organs being [[hypothyroidism]] of the [[thyroid gland]], [[Addison's disease]] of the [[adrenal gland]]s, and [[candida infection]] of body surfaces including the [[oral mucosa|inner lining of the mouth]] and of the [[nail (anatomy)|nail]]s due to dysfunction of [[T helper 17 cell|TH17 cells]], and symptoms often beginning in childhood. Many other autoimmune diseases may also occur.{{sfn|Harrison's|2015|pp=2756-7}} Treatment is directed at the affected organs.{{sfn|Harrison's|2015|pp=2756-7}} ====Thymoma-associated multiorgan autoimmunity==== [[Thymoma-associated multiorgan autoimmunity]] can occur in people with thymoma. In this condition, the T cells developed in the thymus are directed against the tissues of the body. This is because the malignant thymus is incapable of appropriately educating developing thymocytes to eliminate self-reactive T cells. The condition is virtually indistinguishable from [[graft versus host disease]].<ref>{{cite journal | vauthors = Wadhera A, Maverakis E, Mitsiades N, Lara PN, Fung MA, Lynch PJ | title = Thymoma-associated multiorgan autoimmunity: a graft-versus-host-like disease | journal = Journal of the American Academy of Dermatology | volume = 57 | issue = 4 | pages = 683β9 | date = October 2007 | pmid = 17433850 | doi = 10.1016/j.jaad.2007.02.027 }}</ref> ====Myasthenia gravis==== [[Myasthenia gravis]] is an autoimmune disease most often due to antibodies that block [[acetylcholine receptors]], involved in signalling [[neuromuscular junction|between nerves and muscles]].{{sfn|Davidson's|2018|pp=1141-43}} It is often associated with thymic hyperplasia or thymoma,{{sfn|Davidson's|2018|pp=1141-43}} with antibodies produced probably because of T cells that develop abnormally.<ref name=":2">{{cite journal | vauthors = Engels EA | title = Epidemiology of thymoma and associated malignancies | journal = Journal of Thoracic Oncology | volume = 5 | issue = 10 Suppl 4 | pages = S260-5 | date = October 2010 | pmid = 20859116 | pmc = 2951303 | doi = 10.1097/JTO.0b013e3181f1f62d }}</ref> Myasthenia gravis most often develops between young and middle age, causing easy fatiguing of muscle movements.{{sfn|Davidson's|2018|pp=1141-43}} Investigations include demonstrating antibodies (such as against acetylcholine receptors or [[MuSK protein|muscle-specific kinase]]), and [[CT chest|CT scan]] to detect thymoma or thymectomy.{{sfn|Davidson's|2018|pp=1141-43}} With regard to the thymus, removal of the thymus, called [[thymectomy]] may be considered as a treatment, particularly if a thymoma is found.{{sfn|Davidson's|2018|pp=1141-43}} Other treatments include increasing the duration of acetylcholine action at nerve synapses by decreasing the rate of breakdown. This is done by [[acetylcholinesterase inhibitors]] such as [[pyridostigmine]].{{sfn|Davidson's|2018|pp=1141-43}}
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