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

Paul W. McDonald, Kaitlin A. Read, Chandra E. Baker, Ashlyn E. Anderson, Michael D. Powell, André Ballesteros-Tato and Kenneth J. Oestreich ()
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Paul W. McDonald: Virginia Tech Carilion Research Institute
Kaitlin A. Read: Virginia Tech Carilion Research Institute
Chandra E. Baker: Virginia Tech Carilion Research Institute
Ashlyn E. Anderson: Virginia Tech Carilion Research Institute
Michael D. Powell: Virginia Tech Carilion Research Institute
André Ballesteros-Tato: University of Alabama at Birmingham, Birmingham, Alabama 35294, USA
Kenneth J. Oestreich: Virginia Tech Carilion Research Institute

Nature Communications, 2016, vol. 7, issue 1, 1-12

Abstract: Abstract The 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-6Rα 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-6Rα+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.

Date: 2016
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DOI: 10.1038/ncomms10285

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