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首页> 外文期刊>Cellular immunology >Type 1 helper T cells generate CXCL9/10-producing T-bet(+) effector B cells potentially involved in the pathogenesis of rheumatoid arthritis
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Type 1 helper T cells generate CXCL9/10-producing T-bet(+) effector B cells potentially involved in the pathogenesis of rheumatoid arthritis

机译：1型辅助T细胞产生CXCL9 / 10产生的T-BET（+）效应B细胞可能涉及类风湿性关节炎的发病机制

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摘要

Efficacy of B-cell depletion therapy highlights the antibody-independent effector functions of B cells in rheumatoid arthritis (RA). Given type 1 helper T (Th1) cells abundant in synovial fluid (SF) of RA, we have determined whether Th1 cells could generate novel effector B cells. Microarray and qPCR analysis identified CXCL9/10 transcripts as highly expressed genes upon BCR/CD40/IFN-gamma stimulation. Activated Th1 cells promoted the generation of CXCL9/10-producing T-bet+ B cells. Expression of CXCL9/10 was most pronounced in CXCR3+ switched memory B cells. Compared with peripheral blood, SFRA enriched highly activated Th1 cells that coexisted with abundant CXCL9/10-producing T-bet+ B cells. Intriguingly, anti-IFN-gamma antibody and JAK inhibitors significantly abrogated the generation of CXCL9/10-producing T-bet+ B cells. B cell derived CXCL9/10 significantly facilitated the migration of CD4+ T cells. These findings suggest that Th1 cells generate the novel CXCL9/10-producing T-bet+ effector B cells that could be an ideal pathogenic B cell target for RA therapy.
机译：B细胞去除疗法的疗效突出了类风湿关节炎（RA）中B细胞的抗体非依赖性效应器功能。鉴于RA滑液（SF）中富含1型辅助性T（Th1）细胞，我们已经确定Th1细胞是否能产生新的效应B细胞。微阵列和qPCR分析表明，在BCR/CD40/IFNγ刺激下，CXCL9/10转录物是高表达基因。活化的Th1细胞促进产生CXCL9/10的T-bet+B细胞的生成。CXCL9/10的表达在CXCR3+开关记忆B细胞中最为明显。与外周血相比，富含SFRA的高活性Th1细胞与大量产生CXCL9/10的T-bet+B细胞共存。有趣的是，抗IFN-γ抗体和JAK抑制剂显著抑制了产生CXCL9/10的T-bet+B细胞的产生。B细胞衍生的CXCL9/10显著促进CD4+T细胞的迁移。这些发现表明，Th1细胞产生新的产生CXCL9/10的T-bet+效应B细胞，可能是RA治疗的理想致病性B细胞靶点。

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