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Published 7 November 2005. doi:10.1084/jem.20051044
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 202, Number 9, 1289-1300
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ARTICLE

 IL-2 production in developing Th1 cells is regulated by heterodimerization of RelA and T-bet and requires T-bet serine residue 508

Eun Sook Hwang1,2, Jeong-Ho Hong4, and Laurie H. Glimcher2,3

1 Division of Molecular Life Sciences and College of Pharmacy, Ewha Womans University, Seoul, Korea 121-742
2 Department of Immunology and Infectious Diseases, Harvard School of Public Health
3 Department of Medicine, Harvard Medical School, Boston, MA 02115
4 Center for Cancer Research, Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139

CORRESPONDENCE Laurie H. Glimcher: lglimche{at}hsph.harvard.edu OR Eun Sook Hwang: eshwang{at}ewha.ac.kr

Interleukin (IL)-2 is the predominant cytokine that is produced by naive Th cells in a primary response. It is required for proliferation and differentiation of Th precursor cells into effector cells. Initial high-level IL-2 production is followed by its decline, and the concomitant induction of cytokines that are typical of the differentiated state. Although the factors that are responsible for the early induction of IL-2 are well defined, the mechanisms that are responsible for its down-regulation in later stages of Th development have not been studied as much. Previous work from our laboratory revealed a repressor function for the T-box transcription factor, T-bet, in IL-2 gene transcription. Here, we report that T-betS508 is required for the optimal repression of IL-2 production in developing Th1 cells. Phosphorylation of T-betS508 by casein kinase I and glycogen synthase kinase-3 kinases accompanies T-bet's interaction with the RelA nuclear factor–{kappa}B transcription factor. Heterodimerization of T-bet and RelA interferes with the binding of RelA to the IL-2 promoter, and hence, transcriptional activation of the IL-2 gene by RelA.

Abbreviations used: ChIP, chromatin immunoprecipitation; CKI, casein kinase 1; CREB, cyclic AMP response element binding protein; CREM, cyclic AMP resonsive element modulator gene; GSK, glycogen synthase kinase; MS, mass spectrometry; PKA, protein kinase A; S508, serine 508; Thp, Th precursor.


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