Research Group Neuroinflammation and Mucosal Immunology, Max Planck Institute of Biochemistry, Martinsried, Germany.
Front Immunol. 2021 Jun 2;12:668487. doi: 10.3389/fimmu.2021.668487. eCollection 2021.
There is a great interest in developing antigen-specific therapeutic approaches for the treatment of autoimmune diseases without compromising normal immune function. The key challenges are to control all antigen-specific lymphocyte populations that contribute to pathogenic inflammatory processes and to provide long-term protection from disease relapses. Here, we show that myelin oligodendrocyte glycoprotein (MOG)-specific tolerance can be established by ectopic expression of MOG in the immune organs. Using transgenic mice expressing MOG-specific CD4, CD8, and B cell receptors, we show that MOG expression in the bone marrow cells results in impaired development of MOG-specific lymphocytes. Ectopic MOG expression has also resulted in long-lasting protection from MOG-induced autoimmunity. This finding raises hope that transplantation of autoantigen-expressing bone marrow cells as a therapeutic strategy for specific autoantigen-driven autoimmune diseases.
人们对于开发针对自身免疫性疾病的抗原特异性治疗方法非常感兴趣，这种方法不会影响正常的免疫功能。关键的挑战是控制所有导致致病性炎症过程的抗原特异性淋巴细胞群，并提供长期的疾病复发保护。在这里，我们展示了在免疫器官异位表达髓鞘少突胶质细胞糖蛋白（MOG）可以诱导产生 MOG 特异性耐受。利用表达 MOG 特异性 CD4、CD8 和 B 细胞受体的转基因小鼠，我们发现骨髓细胞中 MOG 的表达导致 MOG 特异性淋巴细胞的发育受损。异位 MOG 表达也导致了对 MOG 诱导的自身免疫的长期保护。这一发现为作为特定自身抗原驱动的自身免疫性疾病的治疗策略的表达自身抗原的骨髓细胞移植带来了希望。
