NK1.1+ CD8+ T cells escape TGF-β control and contribute to early microbial pathogen response

Anne L. Ruiz, Saidi M’Homa Soudja, Cyril Deceneux, Grégoire Lauvau and Julien C. Marie ()
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Anne L. Ruiz: Cancer Research Center of Lyon UMR INSERM 1052 CNRS 5286, Immunology, 28 rue Laennec
Saidi M’Homa Soudja: Albert Einstein College of Medicine of Yeshiva University
Cyril Deceneux: Cancer Research Center of Lyon UMR INSERM 1052 CNRS 5286, Immunology, 28 rue Laennec
Grégoire Lauvau: Albert Einstein College of Medicine of Yeshiva University
Julien C. Marie: Cancer Research Center of Lyon UMR INSERM 1052 CNRS 5286, Immunology, 28 rue Laennec

Nature Communications, 2014, vol. 5, issue 1, 1-13

Abstract: Abstract Following microbial pathogen invasion, one of the main challenges for the host is to rapidly control pathogen spreading to avoid vital tissue damage. Here we report that an effector CD8+ T-cell population that expresses the marker NK1.1 undergoes delayed contraction and sustains early anti-microbial protection. NK1.1+ CD8+ T cells are derived from CD8+ T cells during priming, and their differentiation is inhibited by transforming growth factor-β signalling. After their own contraction phase, they form a distinct pool of KLRG1 CD127 double-positive memory T cells and rapidly produce both interferon-γ and granzyme B, providing significant pathogen protection in an antigen-independent manner within only a few hours. Thus, by prolonging the CD8+ T-cell response at the effector stage and by expressing exacerbated innate-like features at the memory stage, NK1.1+ cells represent a distinct subset of CD8+ T cell that contributes to the early control of microbial pathogen re-infections.

Date: 2014
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DOI: 10.1038/ncomms6150

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