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BCL6 orchestrates Tfh cell differentiation via multiple distinct mechanisms
Journal article   Open access   Peer reviewed

BCL6 orchestrates Tfh cell differentiation via multiple distinct mechanisms

Katerina Hatzi, J. Philip Nance, Mark A. Kroenke, Marcella Bothwell, Elias K. Haddad, Ari Melnick and Shane Crotty
The Journal of experimental medicine, v 212(4), pp 539-553
04 Apr 2015
PMID: 25824819
url
https://rupress.org/jem/article-pdf/212/4/539/1013831/jem_20141380.pdfView
Published, Version of Record (VoR) Open

Abstract

Immunology Life Sciences & Biomedicine Medicine, Research & Experimental Research & Experimental Medicine Science & Technology
Follicular helper T cells (Tfh cells) are required for T cell help to B cells, and BCL6 is the defining transcription factor of Tfh cells. However, the functions of BCL6 in Tfh cells have largely remained unclear. Here we defined the BCL6 cistrome in primary human germinal center Tfh cells to assess mechanisms of BCL6 regulation of CD4 T cells, comparing and contrasting BCL6 function in T and B cells. BCL6 primarily acts as a repressor in Tfh cells, and BCL6 binding was associated with control of Tfh cell migration and repression of alternative cell fates. Interestingly, although some BCL6-bound genes possessed BCL6 DNA-binding motifs, many BCL6-bound loci were instead characterized by the presence of DNA motifs for AP1 or STAT. AP1 complexes are key positive downstream mediators of TCR signaling and external stimuli. We show that BCL6 can directly bind AP1, and BCL6 depends on AP1 for recruitment to BCL6-binding sites with AP1 motifs, suggesting that BCL6 subverts AP1 activity. These findings reveal that BCL6 has broad and multifaceted effects on Tfh biology and provide insight into how this master regulator mediates distinct cell context-dependent phenotypes.

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Collaboration types
Domestic collaboration
Web of Science research areas
Immunology
Medicine, Research & Experimental
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