The Journal of Experimental Medicine
Keystone Symposia
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Published 7 February 2005. doi:10.1084/jem.20040733
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 201, Number 3, 397-408
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ARTICLE

 Regulation of T helper type 2 cell differentiation by murine Schnurri-2

Motoko Y. Kimura1, Hiroyuki Hosokawa1, Masakatsu Yamashita1, Akihiro Hasegawa1, Chiaki Iwamura1, Hiroshi Watarai1, Masaru Taniguchi2, Tsuyoshi Takagi3, Shunsuke Ishii3, and Toshinori Nakayama1

1 Department of Immunology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan
2 Laboratory for Immune Regulation, RIKEN Research Center for Allergy and Immunology, Yokohama 230-0045, Japan
3 Laboratory of Molecular Genetics, RIKEN Tsukuba Institute, Ibaraki 305-0074, Japan

CORRESPONDENCE Toshinori Nakayama: tnakayama{at}faculty.chiba-u.jp

Schnurri (Shn) is a large zinc finger protein implicated in cell growth, signal transduction, and lymphocyte development. Vertebrates possess at least three Shn orthologues (Shn-1, Shn-2, and Shn-3), which appear to act within the bone morphogenetic protein, transforming growth factor ß, and activin signaling pathways. However, the physiological functions of the Shn proteins remain largely unknown. In Shn-2–deficient mice, mature peripheral T cells exhibited normal anti–T cell receptor–induced proliferation, although there was dramatic enhancement in the differentiation into T helper type (Th)2 cells and a marginal effect on Th1 cell differentiation. Shn-2–deficient developing Th2 cells showed constitutive activation of nuclear factor {kappa}B (NF-{kappa}B) and enhanced GATA3 induction. Shn-2 was able to compete with p50 NF-{kappa}B for binding to a consensus NF-{kappa}B motif and inhibit NF-{kappa}B–driven promoter activity. Thus, Shn-2 plays a crucial role in the control of Th2 cell differentiation by regulating NF-{kappa}B function.

Abbreviations used: BMDC, bone marrow–derived DC; CFSE, carboxyfluorescein diacetate succinimidyl ester; EMSA, electrophoretic mobility shift assay; Shn, Schnurri; Tg, transgenic; TRAF, TNF receptor–associated factor.


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