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Elife. 2014 May 19;3:e01949. doi: 10.7554/eLife.01949.

T cell-intrinsic role of IL-6 signaling in primary and memory responses.

Author information

1
Department of Immunobiology, Yale University School of Medicine, New Haven, United States.
2
Max Planck Institute for Neurological Research, Cologne, Germany.
3
Department of Biostatistics, Yale School of Public Health, New Haven, United States.
4
Department of Immunobiology, Yale University School of Medicine, New Haven, United States Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, United States ruslan.medzhitov@yale.edu.

Abstract

Innate immune recognition is critical for the induction of adaptive immune responses; however the underlying mechanisms remain incompletely understood. In this study, we demonstrate that T cell-specific deletion of the IL-6 receptor α chain (IL-6Rα) results in impaired Th1 and Th17 T cell responses in vivo, and a defect in Tfh function. Depletion of Tregs in these mice rescued the Th1 but not the Th17 response. Our data suggest that IL-6 signaling in effector T cells is required to overcome Treg-mediated suppression in vivo. We show that IL-6 cooperates with IL-1β to block the suppressive effect of Tregs on CD4(+) T cells, at least in part by controlling their responsiveness to IL-2. In addition, although IL-6Rα-deficient T cells mount normal primary Th1 responses in the absence of Tregs, they fail to mature into functional memory cells, demonstrating a key role for IL-6 in CD4(+) T cell memory formation.DOI: http://dx.doi.org/10.7554/eLife.01949.001.

KEYWORDS:

T cells; cytokines; memory; regulatory T cells

PMID:
24842874
PMCID:
PMC4046568
DOI:
10.7554/eLife.01949
[Indexed for MEDLINE]
Free PMC Article
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