组织蛋白酶 G 在灵长类多发性硬化症模型中的耐受作用：EB 病毒感染的阻断作用。
A Tolerogenic Role of Cathepsin G in a Primate Model of Multiple Sclerosis: Abrogation by Epstein-Barr Virus Infection.
机构信息
Department of Biomedical Sciences of Cells and Systems, University of Groningen, University Medical Center, Groningen, The Netherlands.
Department of Anatomy and Neurosciences, VU Medical Center, Amsterdam, The Netherlands.
出版信息
Arch Immunol Ther Exp (Warsz). 2020 Jun 16;68(4):21. doi: 10.1007/s00005-020-00587-1.
Using a non-human primate model of the autoimmune neuroinflammatory disease multiple sclerosis (MS), we have unraveled the role of B cells in the making and breaking of immune tolerance against central nervous system myelin. It is discussed here that B cells prevent the activation of strongly pathogenic T cells present in the naïve repertoire, which are directed against the immunodominant myelin antigen MOG (myelin oligodendrocyte glycoprotein). Prevention occurs via destructive processing of a critical epitope (MOG34-56) through the lysosomal serine protease cathepsin G. This effective tolerance mechanism is abrogated when the B cells are infected with Epstein-Barr virus, a ubiquitous γ1-herpesvirus that entails the strongest non-genetic risk factor for MS.
使用自身免疫性神经炎症性疾病多发性硬化症（MS）的非人类灵长类动物模型，我们揭示了 B 细胞在中枢神经系统髓鞘针对免疫耐受的建立和打破中的作用。本文讨论了 B 细胞阻止针对免疫优势髓鞘抗原 MOG（髓鞘少突胶质细胞糖蛋白）的幼稚库中存在的强烈致病性 T 细胞的激活。这种有效的耐受机制是通过溶酶体丝氨酸蛋白酶组织蛋白酶 G 对关键表位（MOG34-56）进行破坏性处理来实现的。当 B 细胞感染 Epstein-Barr 病毒（一种普遍存在的γ1-疱疹病毒）时，这种有效的耐受机制会被破坏，而 Epstein-Barr 病毒是 MS 的最强非遗传风险因素。
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