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微生物和自身免疫在神经精神疾病发病机制中的作用。

The role of microbes and autoimmunity in the pathogenesis of neuropsychiatric illness.

机构信息

Department of Epidemiology, Center for Infection and Immunity, Mailman School of Public Health, Columbia University, New York, New York 10032, USA.

出版信息

Curr Opin Rheumatol. 2013 Jul;25(4):488-795. doi: 10.1097/BOR.0b013e32836208de.

DOI:10.1097/BOR.0b013e32836208de
PMID:23656715
Abstract

PURPOSE OF REVIEW

To illustrate how microbes might participate in the pathogenesis of neuropsychiatric illness by triggering the production of autoantibodies that bind to brain targets.

RECENT FINDINGS

Some studies link exposure to infectious agents to development of brain disorders; others have identified autoantibodies in individuals with these conditions without finding evidence of pathogens. Neither line of work demonstrates consistent associations between a specific neuropsychiatric disease and a particular environmental trigger or immune marker. Growing evidence suggests that the microbiome conditions host immunity to microbes and xenobiotics, and regulates autoimmune responses that can affect the central nervous system (CNS). The presence of CNS receptors for cytokines and other immune molecules underscores the importance of brain-immune crosstalk in maintaining normal function. An increased prevalence of familial autoimmunity, exposure to pathogens prenatally and postnatally, and findings of antibrain antibodies is common in disorders as diverse as schizophrenia, obsessive-compulsive disorder and autism, and suggests that differences in exposure timing and genetic vulnerability toward autoimmunity are important determinants of neuropsychiatric outcomes.

SUMMARY

Microbes, both pathogenic and commensal, can induce autoantibodies that bind to brain and affect behavior in susceptible hosts. Interventions that correct the microbial balance or diminish autoantibody binding may be effective in diverse neuropsychiatric conditions mediated by autoimmunity.

摘要

目的综述:通过触发与脑靶标结合的自身抗体的产生,说明微生物如何参与神经精神疾病的发病机制。

最新发现:一些研究将接触传染性病原体与脑疾病的发展联系起来;另一些研究在这些情况下的个体中发现了自身抗体,而没有发现病原体的证据。这两条研究路线都没有证明特定的神经精神疾病与特定的环境触发因素或免疫标志物之间存在一致的关联。越来越多的证据表明,微生物组调节宿主对微生物和外源性物质的免疫,调节可能影响中枢神经系统(CNS)的自身免疫反应。CNS 细胞因子和其他免疫分子受体的存在强调了脑-免疫相互作用在维持正常功能中的重要性。在精神分裂症、强迫症和自闭症等多种疾病中,常见家族自身免疫的患病率增加、产前和产后接触病原体以及发现抗脑抗体,这表明自身免疫的暴露时间和遗传易感性差异是神经精神疾病结果的重要决定因素。

总结:无论是致病性微生物还是共生微生物,都可以诱导与脑结合并影响易感宿主行为的自身抗体。纠正微生物平衡或减少自身抗体结合的干预措施可能对自身免疫介导的多种神经精神疾病有效。

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