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
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...