自身免疫
免疫学
B细胞
发病机制
自身免疫性疾病
下调和上调
生物
免疫系统
抗体
基因
遗传学
作者
Chisato Ono,Shinya Tanaka,Keiko Myouzen,Takeshi Iwasaki,M Takahashi,Yoshinao Oda,Kazuhiko Yamamoto,Yuta Kochi,Yoshihiro Baba
标识
DOI:10.3389/fimmu.2023.1276014
摘要
B cell anergy plays a critical role in maintaining self-tolerance by inhibiting autoreactive B cell activation to prevent autoimmune diseases. Here, we demonstrated that Fc receptor-like 5 (Fcrl5) upregulation contributes to autoimmune disease pathogenesis by disrupting B cell anergy. Fcrl5—a gene whose homologs are associated with human autoimmune diseases—is highly expressed in age/autoimmunity-associated B cells (ABCs), an autoreactive B cell subset. By generating B cell-specific Fcrl5 transgenic mice, we demonstrated that Fcrl5 overexpression in B cells caused systemic autoimmunity with age. Additionally, Fcrl5 upregulation in B cells exacerbated the systemic lupus erythematosus-like disease model. Furthermore, an increase in Fcrl5 expression broke B cell anergy and facilitated toll-like receptor signaling. Thus, Fcrl5 is a potential regulator of B cell-mediated autoimmunity by regulating B cell anergy. This study provides important insights into the role of Fcrl5 in breaking B cell anergy and its effect on the pathogenesis of autoimmune diseases.
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