Transcriptomics

Dataset Information

298

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


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. Treg mRNA profiles in lymph node from 3-week-old Id2fl/flId3fl/fl;Foxp3Cre/Cre (Id2 Id3 double-knockout) and control mice are generated by deep sequencing.

ORGANISM(S): Mus musculus  

SUBMITTER: Manami Itoi   Masaki Miyazaki  Shuwen Chen  Nissi Varki  Kazuko Miyazaki  Aaron N Chang  Marina Miller  David H Broide  Cornelis Murre  Li F Lu 

PROVIDER: E-GEOD-57682 | ArrayExpress | 2014-06-29

SECONDARY ACCESSION(S): SRP041997GSE57682PRJNA247679

REPOSITORIES: GEO, ArrayExpress, ENA

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Publications

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

Miyazaki Masaki M   Miyazaki Kazuko K   Chen Shuwen S   Itoi Manami M   Miller Marina M   Lu Li-Fan LF   Varki Nissi N   Chang Aaron N AN   Broide David H DH   Murre Cornelis C  

Nature immunology 20140629 8


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  ...[more]

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