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Immunity. 2014 Jan 16;40(1):78-90. doi: 10.1016/j.immuni.2013.10.023.

Signaling through the adaptor molecule MyD88 in CD4+ T cells is required to overcome suppression by regulatory T cells.

Author information

  • 1Department of Immunobiology, Yale University, New Haven, CT 06519, USA; Howard Hughes Medical Institute, School of Medicine, Yale University, New Haven, CT 06519, USA. Electronic address: dominik.schenten@yale.edu.
  • 2Department of Immunobiology, Yale University, New Haven, CT 06519, USA; Howard Hughes Medical Institute, School of Medicine, Yale University, New Haven, CT 06519, USA.
  • 3Department of Biostatistics, Yale School of Public Health, New Haven, CT 06520, USA.
  • 4Department of Immunobiology, Yale University, New Haven, CT 06519, USA.
  • 5Max Planck Institute for Neurological Research, Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD) and Center of Molecular Medicine Cologne (CMMC), Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), Institute for Genetics, University of Cologne, 50931 Cologne, Germany.
  • 6Department of Immunobiology, Yale University, New Haven, CT 06519, USA; Howard Hughes Medical Institute, School of Medicine, Yale University, New Haven, CT 06519, USA. Electronic address: ruslan.medzhitov@yale.edu.

Erratum in

  • Immunity. 2014 May 15;40(5):814.

Abstract

Innate immune recognition controls adaptive immune responses through multiple mechanisms. The MyD88 signaling adaptor operates in many cell types downstream of Toll-like receptors (TLRs) and interleukin-1 (IL-1) receptor family members. Cell-type-specific functions of MyD88 signaling remain poorly characterized. Here, we have shown that the T cell-specific ablation of MyD88 in mice impairs not only T helper 17 (Th17) cell responses, but also Th1 cell responses. MyD88 relayed signals of TLR-induced IL-1, which became dispensable for Th1 cell responses in the absence of T regulatory (Treg) cells. Treg cell-specific ablation of MyD88 had no effect, suggesting that IL-1 acts on naive CD4(+) T cells instead of Treg cells themselves. Together, these findings demonstrate that IL-1 renders naive CD4(+) T cells refractory to Treg cell-mediated suppression in order to allow their differentiation into Th1 cells. In addition, IL-1 was also important for the generation of functional CD4(+) memory T cells.

Copyright © 2014 Elsevier Inc. All rights reserved.

PMID:
24439266
[PubMed - indexed for MEDLINE]
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