title: 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.
authors: 1] Department of Molecular Biology, University of California, San Diego, La Jolla, California, USA. [2].
authors: Masaki
authors: M
authors: Miyazaki
authors: 1] Department of Molecular Biology, University of California, San Diego, La Jolla, California, USA. [2].
authors: Kazuko
authors: K
authors: Miyazaki
authors: 1] Department of Molecular Biology, University of California, San Diego, La Jolla, California, USA. [2].
authors: Shuwen
authors: S
authors: Chen
authors: Department of Immunology and Microbiology, Meiji University of Integrative Medicine, Hiyoshi-cho, Kyoto, Japan.
authors: Manami
authors: M
authors: Itoi
authors: Department of Medicine, University of California, San Diego, La Jolla, California, USA.
authors: Marina
authors: M
authors: Miller
authors: Department of Molecular Biology, University of California, San Diego, La Jolla, California, USA.
authors: Li-Fan
authors: LF
authors: Lu
authors: Department of Pathology, University of California, San Diego, La Jolla, California, USA.
authors: Nissi
authors: N
authors: Varki
authors: Center for Computational Biology, Institute for Genomic Medicine, University of California, San Diego, La Jolla, California, USA.
authors: Aaron N
authors: AN
authors: Chang
authors: Department of Medicine, University of California, San Diego, La Jolla, California, USA.
authors: David H
authors: DH
authors: Broide
authors: Department of Molecular Biology, University of California, San Diego, La Jolla, California, USA.
authors: Cornelis
authors: C
authors: Murre
mesh_terms: D000818:Animals; D001483:Base Sequence; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D002454:Cell Differentiation / Q000276:immunology; D002465:Cell Movement / Q000276:immunology; D049109:Cell Proliferation; D005260:Female; D051858:Forkhead Transcription Factors / Q000096:biosynthesis; D005786:Gene Expression Regulation / Q000276:immunology; D049452:Green Fluorescent Proteins / Q000235:genetics; D007249:Inflammation / Q000235:genetics / Q000276:immunology*; D051797:Inhibitor of Differentiation Protein 2 / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology*; D051796:Inhibitor of Differentiation Proteins / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology*; D016753:Interleukin-10 / Q000096:biosynthesis; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D011948:Receptors, Antigen, T-Cell / Q000276:immunology; D054380:Receptors, CXCR5 / Q000096:biosynthesis; D017423:Sequence Analysis, RNA; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*
chemical_list: C513179:CXCR5 protein, mouse; D051858:Forkhead Transcription Factors; C498833:Foxp3 protein, mouse; C556062:IL10 protein, mouse; C497452:Idb2 protein, mouse; D051797:Inhibitor of Differentiation Protein 2; D051796:Inhibitor of Differentiation Proteins; D011948:Receptors, Antigen, T-Cell; D054380:Receptors, CXCR5; D016753:Interleukin-10; C067679:Idb3 protein, mouse; D049452:Green Fluorescent Proteins