精神分裂症的自身免疫模型

ISRN Psychiatry Pub Date : 2012-04-30 Print Date: 2012-01-01 DOI:10.5402/2012/758072
D D Adams, J G Knight, A Ebringer
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引用次数: 4

摘要

精神分裂症具有神秘的因果关系。它没有传染性,不是先天性的,但显示出家族聚集性,孟德尔遗传学表明涉及多个外显率不完全的共显性基因。这是自身免疫性疾病的模式,如甲状腺的Graves病,在这种疾病中,B淋巴细胞的克隆被禁止,并通过分泌自身抗体引起甲状腺毒症,这些自身抗体与甲状腺的垂体促甲状腺激素受体反应。1982年,奈特推测,影响大脑边缘区域神经元功能的自身抗体可能是精神分裂症的原因。如今,这种可能性更大,易患精神分裂症的基因被发现是免疫反应基因,一个在MHC,两个在抗体轻链V基因。免疫反应基因控制免疫系统,决定自身免疫性疾病的遗传风险。对精神分裂症自身免疫基础最简单的测试是在急性病例中用泼尼松进行免疫抑制试验。迫切需要的研究是找到微生物触发因素,正如埃布林格对类风湿性关节炎和强直性脊柱炎所做的那样。这可以通过接种针对触发微生物的疫苗来预防精神分裂症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

The autoimmune model of schizophrenia.

The autoimmune model of schizophrenia.

The autoimmune model of schizophrenia.

The autoimmune model of schizophrenia.

Schizophrenia is of mysterious causation. It is not infectious, not congenital, but shows familial aggregation, the Mendelian genetics indicating involvement of multiple codominant genes with incomplete penetrance. This is the pattern for autoimmune diseases, such as Graves' disease of the thyroid, where forbidden clones of B lymphocytes develop, and cause thyrotoxicosis by secreting autoantibodies that react with the thyroid gland's receptor for thyroid-stimulating hormone from the pituitary gland. In 1982, Knight postulated that autoantibodies affecting the function of neurons in the limbic region of the brain are a possible cause of schizophrenia. Today, this is even more probable, with genes predisposing to schizophrenia having being found to be immune response genes, one in the MHC and two for antibody light chain V genes. Immune response genes govern the immune repertoire, dictating the genetic risk of autoimmune diseases. The simplest test for an autoimmune basis of schizophrenia would be trial of immunosuppression with prednisone in acute cases. The urgent research need is to find the microbial trigger, as done by Ebringer for rheumatoid arthritis and for ankylosing spondylitis. This could lead to prophylaxis of schizophrenia by vaccination against the triggering microbe.

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