CXCR5+PD-1+ follicular helper CD8 T cells control B cell tolerance.,Nature Communications

当前位置： X-MOL 学术 › Nat. Commun. › 论文详情

Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)

CXCR5+PD-1+ follicular helper CD8 T cells control B cell tolerance.
Nature Communications ( IF 14.7 ) Pub Date : 2019-09-27 , DOI: 10.1038/s41467-019-12446-5
Yuhong Chen ₁ , Mei Yu ₁ , Yongwei Zheng ₁ , Guoping Fu ₁ , Gang Xin ₁ , Wen Zhu _{1,

2} , Lan Luo _{1,

3} , Robert Burns ₁ , Quan-Zhen Li ₄ , Alexander L Dent ₅ , Nan Zhu ₁ , Weiguo Cui ₁ , Laurent Malherbe ₆ , Renren Wen ₁ , Demin Wang _{1,

2,

7}

Affiliation

Many autoimmune diseases are characterized by the production of autoantibodies. The current view is that CD4+ T follicular helper (Tfh) cells are the main subset regulating autoreactive B cells. Here we report a CXCR5+PD1+ Tfh subset of CD8+ T cells whose development and function are negatively modulated by Stat5. These CD8+ Tfh cells regulate the germinal center B cell response and control autoantibody production, as deficiency of Stat5 in CD8 T cells leads to an increase of CD8+ Tfh cells, resulting in the breakdown of B cell tolerance and concomitant autoantibody production. CD8+ Tfh cells share similar gene signatures with CD4+ Tfh, and require CD40L/CD40 and TCR/MHCI interactions to deliver help to B cells. Our study thus highlights the diversity of follicular T cell subsets that contribute to the breakdown of B-cell tolerance.

中文翻译：

CXCR5 + PD-1 +卵泡辅助CD8 T细胞控制B细胞耐受性。

许多自身免疫性疾病的特征是自身抗体的产生。目前的观点是CD4 + T卵泡辅助细胞（Tfh）是调节自身反应性B细胞的主要子集。在这里，我们报告CD8 + T细胞的CXCR5 + PD1 + Tfh子集，其发育和功能受到Stat5的负调控。这些CD8 + Tfh细胞调节生发中心B细胞反应并控制自身抗体的产生，因为CD8 T细胞中Stat5的缺乏会导致CD8 + Tfh细胞的增加，从而导致B细胞耐受性下降和伴随的自身抗体产生。CD8 + Tfh细胞与CD4 + Tfh具有相似的基因特征，并且需要CD40L / CD40和TCR / MHCI相互作用才能为B细胞提供帮助。因此，我们的研究突出了导致B细胞耐受性下降的滤泡性T细胞亚群的多样性。

更新日期：2019-09-27

点击分享查看原文

点击收藏

公开下载

阅读更多本刊新发论文本刊介绍/投稿指南