期刊
EUROPEAN JOURNAL OF IMMUNOLOGY
卷 41, 期 8, 页码 2404-2413出版社
WILEY
DOI: 10.1002/eji.201141553
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- Academy of Finland
- Turku Graduate School of Biomedical Sciences
- Finnish-Norwegian Medical Foundation
- Turku University Foundation
- EVO
- Paulo Foundation
- Orion-Farmos Research Foundation
- Moikoinen Cancer Research Foundation
- Emil Aaltonen Foundation
- Finnish Cultural Foundation
- Juliana von Wendt Foundation
- Biocenter Finland
The transcription factor Bcl6 regulates germinal center formation and differentiation of B cells into high-affinity antibody-producing plasma cells. The direct double-negative regulatory circuit between Bcl6 and Blimp-1 is well established. We now reveal alternative mechanisms for Bcl6-mediated regulation of B-cell differentiation to plasma cells and show with DT40 cells that Bcl6 directly promotes the expression of Bach2, a known suppressor of Blimp-1. Moreover, Bcl6 suppresses Blimp-1 expression through direct binding to the IRF4 gene, as well as by promoting the expression of MITF, a known suppressor of IRF4. We also provide evidence that Bcl6 is needed for the expression of AID and UNG, the indispensable proteins for somatic hypermutation and class-switch recombination, and UNG appears to be a direct Bcl6 target. Our findings reveal a complex regulatory network in which Bcl6 acts as a key element dictating the transition of DT40 B cells to plasma cells.
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