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Nat Immunol. 2014 Aug;15(8):767-76. doi: 10.1038/ni.2928. Epub 2014 Jun 29.

Id2 and Id3 maintain the regulatory T cell pool to suppress inflammatory disease.

Author information

1
1] Department of Molecular Biology, University of California, San Diego, La Jolla, California, USA. [2].
2
Department of Immunology and Microbiology, Meiji University of Integrative Medicine, Hiyoshi-cho, Kyoto, Japan.
3
Department of Medicine, University of California, San Diego, La Jolla, California, USA.
4
Department of Molecular Biology, University of California, San Diego, La Jolla, California, USA.
5
Department of Pathology, University of California, San Diego, La Jolla, California, USA.
6
Center for Computational Biology, Institute for Genomic Medicine, University of California, San Diego, La Jolla, California, USA.

Abstract

Regulatory T (Treg) cells suppress the development of inflammatory disease, but our knowledge of transcriptional regulators that control this function remains incomplete. Here we show that expression of Id2 and Id3 in Treg cells was required to suppress development of fatal inflammatory disease. We found that T cell antigen receptor (TCR)-driven signaling initially decreased the abundance of Id3, which led to the activation of a follicular regulatory T (TFR) cell-specific transcription signature. However, sustained lower abundance of Id2 and Id3 interfered with proper development of TFR cells. Depletion of Id2 and Id3 expression in Treg cells resulted in compromised maintenance and localization of the Treg cell population. Thus, Id2 and Id3 enforce TFR cell checkpoints and control the maintenance and homing of Treg cells.

PMID:
24973820
PMCID:
PMC4365819
DOI:
10.1038/ni.2928
[Indexed for MEDLINE]
Free PMC Article

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