Institute of Clinical Neuroimmunology, University Hospital, LMU Munich and Biomedical Center (BMC), Faculty of Medicine, LMU Munich, Germany.
Institute of Clinical Neuroimmunology, University Hospital, LMU Munich and Biomedical Center (BMC), Faculty of Medicine, LMU Munich, Germany; Emeritus Group Neuroimmunology, Max Planck Institute of Biological Intelligence, Germany.
Neurotherapeutics. 2024 Oct;21(6):e00442. doi: 10.1016/j.neurot.2024.e00442. Epub 2024 Sep 4.
Brain antigen-specific autoreactive T cells seem to play a key role in inducing inflammation in the central nervous system (CNS), a characteristic feature of human multiple sclerosis (MS). These T cells are generated within the thymus, where they escape negative selection and become integrated into the peripheral immune repertoire of immune cells. Typically, these autoreactive T cells rest in the periphery without attacking the CNS. When autoimmune T cells enter gut-associated lymphatic tissue (GALT), they may be stimulated by the microbiota and its metabolites. After activation, the cells migrate into the CNS through the blood‒brain barrier, become reactivated upon interacting with local antigen-presenting cells, and induce inflammatory lesions within the brain parenchyma. This review describes how microbiota influence autoreactive T cells during their life, starting in the thymus, migrating through the periphery and inducing inflammation in their target organ, the CNS.
脑抗原特异性自身反应性 T 细胞似乎在诱导中枢神经系统 (CNS) 炎症中发挥关键作用,这是人类多发性硬化症 (MS) 的一个特征。这些 T 细胞在胸腺中产生,在那里它们逃避负选择并整合到免疫细胞的外周免疫库中。通常,这些自身反应性 T 细胞在不攻击中枢神经系统的情况下停留在外周。当自身免疫 T 细胞进入肠道相关淋巴组织 (GALT) 时,它们可能会被微生物群及其代谢物刺激。激活后,细胞通过血脑屏障进入中枢神经系统,与局部抗原呈递细胞相互作用后重新激活,并在脑实质内诱导炎症病变。本综述描述了微生物群如何在其一生中影响自身反应性 T 细胞,从胸腺开始,通过外周迁移,并在其靶器官中枢神经系统中引发炎症。