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BCL6 controls contact-dependent help delivery during follicular T-B cell interactions
Immunity ( IF 32.4 ) Pub Date : 2021-08-30 , DOI: 10.1016/j.immuni.2021.08.003
Dan Liu 1 , Jiacong Yan 2 , Jiahui Sun 1 , Bo Liu 1 , Weiwei Ma 3 , Ye Li 3 , Xingxing Shao 2 , Hai Qi 4
Affiliation  

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.



中文翻译:

BCL6 在滤泡 TB 细胞相互作用期间控制依赖于接触的帮助传递

BCL6 是毛囊 T 辅助 (Tfh) 细胞发育以支持生发中心 (GC) 形成所必需的。然而,尚不清楚 BCL6 编程的哪些独特功能可以解释其在 T 细胞中对 GC 形成的绝对必要性。我们发现一个Bcl6等位基因的消融不会明显改变早期 T 细胞活化和滤泡定位,但会抑制 GC 形成和 Tfh 细胞维持。BCL6 影响 Tfh 钙信号,还控制 Tfh 与 B 细胞的 CD40L 纠缠和递送。在体内TB 细胞相互作用强度改变后的数小时内,BCL6 蛋白的数量和 Tfh 细胞的标称频率发生显着变化,而由于 BCL6 单倍体不足,CD40L 过表达纠正了有缺陷的 GC 形成和 Tfh 细胞维持。我们的结果揭示了 Tfh 细胞中 BCL6 的功能,这对于 GC 形成至关重要,并表明 BCL6 有助于以 T 细胞非自主方式维持 Tfh 细胞表型。

更新日期:2021-10-12
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