Excessive immunoglobulin E (IgE) responses are responsible for allergic hypersensitivity disorders and are implicated in other human diseases such as hyper-IgE syndrome and AIDS. In normal individuals IgE expression is tightly regulated, but the mechanisms that control this regulation have been poorly understood. In the December 16 Nature Immunology, Manabu Sugai and colleagues at Kyoto University, Japan, show that Id2 protein (a negative regulators of basic helix-loop-helix transcription factors) also have an essential role in the negative regulation of IgE class switching (Nature Immunology doi:10.1038/ni874, December 16, 2002).

Sugai et al. developed a mouse line deficient in Id2 and observed that B cells from Id2–/– mice preferentially switch to IgE. B cells lacking Id2 had increased E2A activity, which led to specific enhancement of germline transcription of the immunoglobulin εlocus. In addition, they showed that Id2 was induced in wild-type B cells by transforming growth...

Interested in reading more?

Become a Member of

Receive full access to more than 35 years of archives, as well as TS Digest, digital editions of The Scientist, feature stories, and much more!