| Literature DB >> 27487330 |
Yew Ann Leong1, Yaping Chen1, Hong Sheng Ong1, Di Wu2, Kevin Man3,4, Claire Deleage5, Martina Minnich6, Benjamin J Meckiff7, Yunbo Wei8, Zhaohua Hou8, Dimitra Zotos3,4, Kevin A Fenix9, Anurag Atnerkar1, Simon Preston3,4, Jeffrey G Chipman10, Greg J Beilman10, Cody C Allison3,4, Lei Sun11, Peng Wang11, Jiawei Xu12, Jesse G Toe3,4, Hao K Lu13, Yong Tao14, Umaimainthan Palendira15, Alexander L Dent16, Alan L Landay17, Marc Pellegrini3,4, Iain Comerford9, Shaun R McColl9, Timothy W Schacker18, Heather M Long7, Jacob D Estes5, Meinrad Busslinger6, Gabrielle T Belz3,4, Sharon R Lewin13,19, Axel Kallies3,4, Di Yu1,8,20.
Abstract
During unresolved infections, some viruses escape immunological control and establish a persistant reservoir in certain cell types, such as human immunodeficiency virus (HIV), which persists in follicular helper T cells (TFH cells), and Epstein-Barr virus (EBV), which persists in B cells. Here we identified a specialized group of cytotoxic T cells (TC cells) that expressed the chemokine receptor CXCR5, selectively entered B cell follicles and eradicated infected TFH cells and B cells. The differentiation of these cells, which we have called 'follicular cytotoxic T cells' (TFC cells), required the transcription factors Bcl6, E2A and TCF-1 but was inhibited by the transcriptional regulators Blimp1, Id2 and Id3. Blimp1 and E2A directly regulated Cxcr5 expression and, together with Bcl6 and TCF-1, formed a transcriptional circuit that guided TFC cell development. The identification of TFC cells has far-reaching implications for the development of strategies to control infections that target B cells and TFH cells and to treat B cell-derived malignancies.Entities:
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Year: 2016 PMID： 27487330 DOI： 10.1038/ni.3543
Source DB: PubMed Journal: Nat Immunol ISSN： 1529-2908 Impact factor: 25.606