The Journal of Experimental Medicine
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Published online August 25, 2008
doi:10.1084/jem.20080526
The Journal of Experimental Medicine, Vol. 205, No. 9, 1959-1965
The Rockefeller University Press, 0022-1007 $30.00
© 2008 Martins et al.
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BRIEF DEFINITIVE REPORT

 Blimp-1 directly represses Il2 and the Il2 activator Fos, attenuating T cell proliferation and survival

Gislâine A. Martins1, Luisa Cimmino2, Jerry Liao1, Erna Magnusdottir3, and Kathryn Calame1,4

1 Department of Microbiology, 2 The Institute of Human Nutrition, 3 Department of Biological Sciences, and 4 Department of Biochemistry and Molecular Biophysics, Columbia University College of Physicians and Surgeons, New York, NY 10032

CORRESPONDENCE Kathryn Calame: klc1{at}columbia.edu OR Gislâine A. Martins martinsg{at}cshs.org

Mice with a T cell–specific deletion of Prdm1, encoding Blimp-1, have aberrant T cell homeostasis and develop fatal colitis. In this study, we show that one critical activity of Blimp-1 in T cells is to repress IL-2, and that it does so by direct repression of Il2 transcription, and also by repression of Fos transcription. Using these mechanisms Blimp-1 participates in an autoregulatory loop by which IL-2 induces Prdm1 expression and thus represses its own expression after T cell activation, ensuring that the immune response is appropriately controlled. This activity of Blimp-1 is important for cytokine deprivation–induced T cell death and for attenuating T cell proliferation in antigen-specific responses both in vitro and in vivo.

G.A. Martins' present address is Inflammatory Bowel Disease Center, Cedars-Sinai Medical Center, Los Angeles, CA 90048.

© 2008 Martins et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).


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