Regulation of B cell fate by chronic activity of the IgE B cell receptor

Zhiyong Yang, Marcus J. Robinson, Xiangjun Chen, Geoffrey A. Smith, Jack Taunton, Wanli Liu, Christopher D C Allen

Research output: Contribution to journalArticleResearchpeer-review

16 Citations (Scopus)

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.

Original languageEnglish
Article numbere21238
Number of pages31
JournaleLife
Volume5
Issue numberDECEMBER2016
DOIs
Publication statusPublished - 9 Dec 2016
Externally publishedYes

Cite this

Yang, Z., Robinson, M. J., Chen, X., Smith, G. A., Taunton, J., Liu, W., & Allen, C. D. C. (2016). Regulation of B cell fate by chronic activity of the IgE B cell receptor. eLife, 5(DECEMBER2016), [e21238]. https://doi.org/10.7554/eLife.21238.001
Yang, Zhiyong ; Robinson, Marcus J. ; Chen, Xiangjun ; Smith, Geoffrey A. ; Taunton, Jack ; Liu, Wanli ; Allen, Christopher D C. / Regulation of B cell fate by chronic activity of the IgE B cell receptor. In: eLife. 2016 ; Vol. 5, No. DECEMBER2016.
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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.",
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Yang, Z, Robinson, MJ, Chen, X, Smith, GA, Taunton, J, Liu, W & Allen, CDC 2016, 'Regulation of B cell fate by chronic activity of the IgE B cell receptor', eLife, vol. 5, no. DECEMBER2016, e21238. https://doi.org/10.7554/eLife.21238.001

Regulation of B cell fate by chronic activity of the IgE B cell receptor. / Yang, Zhiyong; Robinson, Marcus J.; Chen, Xiangjun; Smith, Geoffrey A.; Taunton, Jack; Liu, Wanli; Allen, Christopher D C.

In: eLife, Vol. 5, No. DECEMBER2016, e21238, 09.12.2016.

Research output: Contribution to journalArticleResearchpeer-review

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Yang Z, Robinson MJ, Chen X, Smith GA, Taunton J, Liu W et al. Regulation of B cell fate by chronic activity of the IgE B cell receptor. eLife. 2016 Dec 9;5(DECEMBER2016). e21238. https://doi.org/10.7554/eLife.21238.001