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- Title
Regulation of B cell fate by chronic activity of the IgE B cell receptor.
- Authors
Zhiyong Yang; Robinson, Marcus J.; Xiangjun Chen; Smith, Geoffrey A.; Taunton, Jack; Wanli Liu; Allen, Christopher D. C.
- Abstract
IgE can trigger potent allergic responses, yet the mechanisms regulating IgE production are poorly understood. Here we reveal that IgE+ B cells are constrained by chronic activity of the IgE B cell receptor (BCR). In the absence of cognate antigen, the IgE BCR promoted terminal differentiation of B cells into plasma cells (PCs) under cell culture conditions mimicking T cell help. This antigen-independent PC differentiation involved multiple IgE domains and Syk, CD19, BLNK, Btk, and IRF4. Disruption of BCR signaling in mice led to consistently exaggerated IgE+ germinal center (GC) B cell but variably increased PC responses. We were unable to confirm reports that the IgE BCR directly promoted intrinsic apoptosis. Instead, IgE+ GC B cells exhibited poor antigen presentation and prolonged cell cycles, suggesting reduced competition for T cell help. We propose that chronic BCR activity and access to T cell help play critical roles in regulating IgE responses.
- Subjects
B cells; IMMUNOGLOBULIN E; B cell receptors; B cell differentiation; IMMUNOREGULATION; CELLULAR signal transduction; PHYSIOLOGY
- Publication
eLife, 2016, p1
- ISSN
2050-084X
- Publication type
Article
- DOI
10.7554/eLife.21238