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Article
Nature Immunology  4, 25 - 30 (2002)
Published online: 16 December 2002; | doi:10.1038/ni874

Essential role of Id2 in negative regulation of IgE class switching

Manabu Sugai1, Hiroyuki Gonda1, 2, Takashi Kusunoki3, Tomoya Katakai1, Yoshifumi Yokota4 & Akira Shimizu1, 2

1  Center for Molecular Biology and Genetics, Kyoto University, Shogoin-Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan.

2  Translational Research Center, Kyoto University Hospital, 54 Shogoin-Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan.

3  Department of Pediatrics, Graduate School of Medicine, Kyoto University, 54 Shogoin-Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan.

4  Department of Biochemistry, Fukui Medical University, 23-3 Shimoaizuki, Matsuoka, Fukui 910-1193, Japan.

Correspondence should be addressed to Akira Shimizu shimizu@virus.kyoto-u.ac.jp
Serum concentrations of immunoglobulin E (IgE) in normal circumstances are kept much lower than those of other Ig isotypes to avoid allergic reactions. B cells lacking Id2 have increased E2A activity, which leads to specific enhancement of germline transcription of the immunoglobulin epsilon locus. As a consequence, Id2-deficient B cells undergo class switch recombination (CSR) to IgE at a much higher frequency than wild-type B cells. In contrast, Id2 is induced in wild-type B cells by transforming growth factor-beta1 (TGF-beta1) and suppresses IgE CSR. Our results provide evidence for the inhibitory and selective role of Id2 in IgE CSR in response to TGF-beta1. Id2 might act as molecular safeguard to suppress IgE CSR to prevent serious complications such as allergic hypersensitivity during the normal course of immune responses.

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Nature Immunology
ISSN: 1529-2908
EISSN: 1529-2916
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