细胞生物学
癌症研究
免疫系统
炎症
化学
细胞因子
细胞
白细胞介素2受体
作者
Qiu-Hui Zeng,Yuan Wei,Xiang-Ming Lao,Dong-Ping Chen,Chun-Xiang Huang,Qian-Yi Lin,Min He,Yuan Liao,Limin Zheng,Bo Li,Guang-Bo Zhang,Yun Chen,Dong-Ming Kuang
出处
期刊:Science Advances
[American Association for the Advancement of Science (AAAS)]
日期:2020-09-01
卷期号:6 (37)
被引量:6
标识
DOI:10.1126/sciadv.abb6296
摘要
B cells constitute abundant cellular components in inflamed human tissues, but their role in pathogenesis of inflammatory T helper (TH) subsets is still unclear. Here, we demonstrate that B cells, particularly resting naive B cells, have a previously unrecognized helper function that is involved in shaping the metabolic process and subsequent inflammatory differentiation of T-cell receptor–primed TH cells. ICOS/ICOSL axis–mediated glucose incorporation and utilization were crucial for inflammatory TH subset induction by B cells, and activation of mTOR was critical for T cell glycolysis in this process. Consistently, upon encountering ICOSL+ B cells, activated effector memory TH cells from patients with rheumatoid arthritis or systemic lupus erythematosus spontaneously differentiated into inflammatory TH subsets. Immunotherapy using rituximab that specifically depleted B cells in patients with rheumatoid arthritis efficiently abrogated the capabilities of memory TH cells to incorporate and use glucose, thereby impairing the pathogenic differentiation of inflammatory TH subsets.
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