Article abstract


Nature Immunology 8, 1236 - 1245 (2007)
Published online: 30 September 2007 | doi:10.1038/ni1514

COP9 signalosome subunit 8 is essential for peripheral T cell homeostasis and antigen receptor–induced entry into the cell cycle from quiescence

Suchithra Menon1,4, Hongbo Chi2,3,4, Huiyong Zhang1, Xing Wang Deng1, Richard A Flavell2 & Ning Wei1


Engagement of antigen receptors triggers the proliferation and functional activation of lymphocytes. Here we report that T cell homeostasis and antigen-induced responses require the COP9 signalosome (CSN), a regulator of the ubiquitin-proteasome system. Conditional deletion of the CSN subunit Csn8 in peripheral T lymphocytes disrupted formation of the CSN complex, reduced T cell survival and proliferation in vivo and impaired antigen-induced production of interleukin 2. Moreover, Csn8-deficient T cells showed defective entry into the cell cycle from the G0 quiescent state. This phenotype was associated with a lack of signal-induced expression of cell cycle–related genes, including G1 cyclins and cyclin-dependent kinases, and with excessive induction of p21Cip1. Our data define a CSN-dependent pathway of transcriptional control that is essential for antigen-induced initiation of T cell proliferation.

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  1. Department of Molecular, Cellular and Developmental Biology, Yale University, New Haven, Connecticut 06511, USA.
  2. Howard Hughes Medical Institute, Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
  3. Department of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.
  4. These authors contributed equally to this work.

Correspondence to: Ning Wei1 e-mail: ning.wei@yale.edu

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