Berer Kerstin, Krishnamoorthy Gurumoorthy
Department of Neuroimmunology, Max Planck Institute of Neurobiology, 82152 Martinsried, Germany.
FEBS Lett. 2014 Nov 17;588(22):4207-13. doi: 10.1016/j.febslet.2014.04.007. Epub 2014 Apr 18.
Not much is known about the initial events leading to the development of the central nervous system (CNS)-specific autoimmune disorder Multiple Sclerosis (MS). Environmental factors are suspected to trigger the pathogenic events in people with genetic disease susceptibility. Historically, many infectious microbes were linked to MS, but no infection has ever been demonstrated to be the cause of the disease. Recent emerging evidence from animal models of MS suggests a causal link with resident commensal bacteria. Microbial organisms may trigger the activation of CNS-specific, auto-aggressive lymphocytes either through molecular mimicry or via bystander activation. In addition, several gut microbial metabolites and bacterial products may interact with the immune system to modulate CNS autoimmunity.
关于导致中枢神经系统(CNS)特异性自身免疫性疾病多发性硬化症(MS)发展的初始事件,人们了解得并不多。环境因素被怀疑会引发具有遗传疾病易感性人群中的致病事件。从历史上看,许多传染性微生物都与MS有关,但从未证明有任何感染是该疾病的病因。最近来自MS动物模型的新证据表明与常驻共生细菌存在因果关系。微生物可能通过分子模拟或旁观者激活来触发CNS特异性自身攻击性淋巴细胞的激活。此外,几种肠道微生物代谢产物和细菌产物可能与免疫系统相互作用,以调节中枢神经系统自身免疫。