Department of Dermatology, The University of Tokyo Graduate School of Medicine, Tokyo, Japan.
Laboratory of Radiology and Biomedical Engineering, The University of Tokyo Graduate School of Medicine, Tokyo, Japan.
Elife. 2021 Dec 2;10:e67209. doi: 10.7554/eLife.67209.
Despite antigen affinity of B cells varying from cell to cell, functional analyses of antigen-reactive B cells on individual B cells are missing due to technical difficulties. Especially in the field of autoimmune diseases, promising pathogenic B cells have not been adequately studied to date because of its rarity. In this study, functions of autoantigen-reactive B cells in autoimmune disease were analyzed at the single-cell level. Since topoisomerase I is a distinct autoantigen, we targeted systemic sclerosis as autoimmune disease. Decreased and increased affinities for topoisomerase I of topoisomerase I-reactive B cells led to anti-inflammatory and pro-inflammatory cytokine production associated with the inhibition and development of fibrosis, which is the major symptom of systemic sclerosis. Furthermore, inhibition of pro-inflammatory cytokine production and increased affinity of topoisomerase I-reactive B cells suppressed fibrosis. These results indicate that autoantigen-reactive B cells contribute to the disease manifestations in autoimmune disease through their antigen affinity.
尽管 B 细胞的抗原亲和力在细胞间存在差异,但由于技术困难,针对单个 B 细胞上的抗原反应性 B 细胞进行功能分析仍然缺失。特别是在自身免疫性疾病领域,由于其罕见性,迄今为止,有前途的致病性 B 细胞尚未得到充分研究。在这项研究中,我们在单细胞水平上分析了自身抗原反应性 B 细胞在自身免疫性疾病中的功能。由于拓扑异构酶 I 是一种独特的自身抗原,我们将系统性硬化症作为自身免疫性疾病的靶点。拓扑异构酶 I 反应性 B 细胞对拓扑异构酶 I 的亲和力降低和增加导致与纤维化的抑制和发展相关的抗炎和促炎细胞因子产生,纤维化是系统性硬化症的主要症状。此外,抑制促炎细胞因子的产生和增加拓扑异构酶 I 反应性 B 细胞的亲和力可抑制纤维化。这些结果表明,自身抗原反应性 B 细胞通过其抗原亲和力对自身免疫性疾病的临床表现做出贡献。