Immunoglobulin E (IgE) is central to triggering allergy; therefore, IgE+ B cells must be tightly controlled and their numbers must be kept in check. In eLife, Allen and colleagues study the IgE B cell antigen receptor (BCR) to gain insight into how it regulates the fate and frequency of IgE+ B cells. They find that the IgE BCR is weakly active even in the absence of cognate ligand and drives a pathway that involves the signaling molecules Syk, BLNK and Btk. This signaling promotes the differentiation of B cells into low-affinity plasma cells, but the authors find no evidence that it triggers apoptosis. This characteristic signaling activity of the IgE BCR is dependent in part on a short and distinctive membrane-proximal segment called the 'migis'. The unique properties of the IgE BCR are therefore hardwired to avoid the generation of large numbers of potentially harmful high-affinity IgE molecules.

eLife (9 December 2016) http://dx.doi.org/10.7554/eLife.21238