Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 211, Issue 11, Pages 2169-2181Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20140425
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Funding
- National Health and Medical Research Council (NHMRC) of Australia [575500, APP1054925]
- Victorian State Government Operational Infrastructure Support
- Australian Government NHMRC IRIIS
- Intramural Research Program of the National Institutes of Health, National Institute of Allergy and Infectious Diseases
- NHMRC
- Leukaemia Foundation
- Australian Research Council Future Fellowship
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Activated B cells undergo immunoglobulin class-switch recombination (CSR) and differentiate into antibody-secreting plasma cells. The distinct transcriptomes of B cells and plasma cells are maintained by the antagonistic influences of two groups of transcription factors: those that maintain the B cell program, including BCL6 and PAX5, and plasma cell-promoting factors, such as IRF4 and BLIMP-1. We show that the complex of IRF8 and PU.1 controls the propensity of B cells to undergo CSR and plasma cell differentiation by concurrently promoting the expression of BCL6 and PAX5 and repressing AID and BLIMP-1. As the PU.1-IRF8 complex functions in a reciprocal manner to IRF4, we propose that concentration-dependent competition between these factors controls B cell terminal differentiation.
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