Journal
CELL REPORTS
Volume 19, Issue 3, Pages 461-470Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2017.03.060
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Funding
- National Health and Medical Research Council (NHMRC) project grant [1057707]
- NHMRC program grant [1054925]
- Leukaemia Foundation
- NHMRC Career Development Fellowship [1108066]
- NHMRC Research Fellowships [1060675, 1058892]
- Multiple Myeloma Research Foundation
- European Molecular Biology Organization [ALTF 1337-2010]
- Australian Research Council Future Fellowships [FT110100283, FT130100708]
- National Health and Medical Research Council of Australia [1057707, 1108066, 1060675] Funding Source: NHMRC
- Australian Research Council [FT110100283] Funding Source: Australian Research Council
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Humoral immune responses are tailored to the invading pathogen through regulation of key transcription factors and their networks. This is critical to establishing effective antibody-mediated responses, yet it is unknown how B cells integrate pathogeninduced signals to drive or suppress transcriptional programs specialized for each class of pathogen. Here, we detail the key role of the transcription factor c-Myb in regulating the T-bet-mediated anti-viral program. Deletion of c-Myb in mature B cells significantly increased serum IgG2c and CXCR3 expression by upregulating T-bet, normally suppressed during Th2-cell-mediated responses. Enhanced expression of T-bet resulted in aberrant plasma cell differentiation within the germinal center, mediated by CXCR3 expression. These findings identify a dual role for c-Myb in limiting inappropriate effector responses while coordinating plasma cell differentiation with germinal center egress. Identifying such intrinsic regulators of specialized antibody responses can assist in vaccine design and therapeutic intervention in B-cell-mediated immune disorders.
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