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International Immunology Advance Access originally published online on May 9, 2007
International Immunology 2007 19(6):755-762; doi:10.1093/intimm/dxm042
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© The Japanese Society for Immunology. 2007. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Schnurri-2 regulates Th2-dependent airway inflammation and airway hyperresponsiveness

Chiaki Iwamura, Motoko Y. Kimura, Kenta Shinoda, Yusuke Endo, Akihiro Hasegawa, Masakatsu Yamashita and Toshinori Nakayama

Department of Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan

Correspondence to: T. Nakayama; E-mail: tnakayama{at}faculty.chiba-u.jp

Schnurri (Shn)-2 is a large zinc finger-containing protein, which plays a critical role in cell growth, signal transduction and lymphocyte development. In Shn-2-deficient (Shn-2–/–) CD4 T cells, the activation of nuclear factor-{kappa}B is up-regulated and their ability to differentiate into Th2 is enhanced. Here, we extend our investigation and demonstrate that Shn-2 regulates Th2 responses in vivo using an ovalbumin-induced allergic asthma model. Eosinophilic inflammation, mucus hyperproduction and airway hyperresponsiveness (AHR) were all enhanced in Shn-2–/– mice. Moreover, eosinophilic infiltration and AHR were enhanced in mice given a transfer of Shn-2–/– effector Th2. Shn-2 in Th2 is thus considered to play an important role as a negative regulator in allergic airway inflammation.

Keywords: asthma, NF-{kappa}B, Schnurri-2-deficient mice

Transmitting editor: A. Singer

Received 23 November 2006, accepted 16 March 2007.


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