IL-7 signalling represses Bcl-6 and the TFH gene Program

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dc.contributorVirginia Techen
dc.contributor.authorMcDonald, Paul W.en
dc.contributor.authorRead, Kaitlin A.en
dc.contributor.authorBaker, Chandra E.en
dc.contributor.authorAnderson, Ashlyn E.en
dc.contributor.authorPowell, Michael D.en
dc.contributor.authorBallesteros-Tato, Andréen
dc.contributor.authorOestreich, Kenneth J.en
dc.date.accessioned2017-03-13T17:13:40Zen
dc.date.available2017-03-13T17:13:40Zen
dc.date.issued2016-01-08en
dc.description.abstractThe transcriptional repressor Bcl-6 is linked to the development of both CD4⁺ T follicular helper (TFH) and central memory T (TCM) cells. Here, we demonstrate that in response to decreased IL-2 signalling, T helper 1 (TH1) cells upregulate Bcl-6 and co-initiate TFH- and TCM-like gene programs, including expression of the cytokine receptors IL-6R∝ and IL-7R. Exposure of this potentially bi-potent cell population to IL-6 favours the TFH gene program, whereas IL-7 signalling represses TFH-associated genes including Bcl6 and Cxcr5, but not the TCM-related genes Klf2 and Sell. Mechanistically, IL-7-dependent activation of STAT5 contributes to Bcl-6 repression. Importantly, antigen-specific IL-6R∝⁺IL-7R⁺ CD4⁺ T cells emerge from the effector population at late time points post influenza infection. These data support a novel role for IL-7 in the repression of the TFH gene program and evoke a divergent regulatory mechanism by which post-effector TH1 cells may contribute to long-term cell-mediated and humoral immunity.en
dc.format.mimetypeapplication/pdfen
dc.identifier.doihttps://doi.org/10.1038/ncomms10285en
dc.identifier.urihttp://hdl.handle.net/10919/76627en
dc.identifier.volume7en
dc.language.isoen_USen
dc.publisherNatureen
dc.rightsCreative Commons Attribution 4.0 Internationalen
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en
dc.titleIL-7 signalling represses Bcl-6 and the TFH gene Programen
dc.title.serialNature Communicationsen
dc.typeArticle - Refereeden
dc.type.dcmitypeTexten

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