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BCL6控制滤泡T-B细胞相互作用过程中接触依赖性的辅助传递
作者:小柯机器人 发布时间:2021/8/31 15:35:38

清华大学祁海团队发现,BCL6控制滤泡T-B细胞相互作用过程中接触依赖性的辅助传递。相关论文于2021年8月30日在线发表在《免疫》杂志上。

研究人员发现,一个BCL6等位基因的敲除并没有明显改变早期T细胞的激活和滤泡的定位,但抑制了生发中心(GC)的形成和滤泡T辅助(Tfh)细胞的维持。BCL6影响了Tfh的钙信号传导,也控制了Tfh与B细胞的纠缠和CD40L的传递。BCL6蛋白的数量和Tfh细胞的名义频率在体内T-B细胞相互作用的强度改变后的几个小时内发生了明显的变化,而CD40L的过量表达纠正了由于BCL6单倍体功能不足而造成的GC形成和Tfh细胞维持的缺陷。

这些结果揭示了BCL6在Tfh细胞中的功能对GC的形成至关重要,并表明BCL6有助于以T细胞非自主的方式维持Tfh细胞的表型。

据悉,Tfh细胞的发育需要BCL6来支持生发中心(GC)的形成。然而,目前还不清楚BCL6的哪些独特功能可以解释它在T细胞中对GC形成的绝对重要性。

附:英文原文

Title: BCL6 controls contact-dependent help delivery during follicular T-B cell interactions

Author: Dan Liu, Jiacong Yan, Jiahui Sun, Bo Liu, Weiwei Ma, Ye Li, Xingxing Shao, Hai Qi

Issue&Volume: 2021-08-30

Abstract: BCL6 is required for development of follicular T helper (Tfh) cells to support germinal center (GC) formation. However, it is not clear what unique functions programmed by BCL6 can explain its absolute essentiality in T cells for GC formation. We found that ablation of one Bcl6 allele did not appreciably alter early T cell activation and follicular localization but inhibited GC formation and Tfh cell maintenance. BCL6 impinged on Tfh calcium signaling and also controlled Tfh entanglement with and CD40L delivery to B cells. Amounts of BCL6 protein and nominal frequencies of Tfh cells markedly changed within hours after strengths of T-B cell interactions were altered in vivo, while CD40L overexpression rectified both defective GC formation and Tfh cell maintenance because of the BCL6 haploinsufficiency. Our results reveal BCL6 functions in Tfh cells that are essential for GC formation and suggest that BCL6 helps maintain Tfh cell phenotypes in a T cell non-autonomous manner.

DOI: 10.1016/j.immuni.2021.08.003

Source: https://www.cell.com/immunity/fulltext/S1074-7613(21)00333-2

期刊信息

Immunity:《免疫》,创刊于1994年。隶属于细胞出版社,最新IF:21.522
官方网址:https://www.cell.com/immunity/home
投稿链接:https://www.editorialmanager.com/immunity/default.aspx