期刊
NATURE IMMUNOLOGY
卷 14, 期 4, 页码 380-388出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.2543
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资金
- US National Cancer Institute [R01 104348]
- Burroughs Wellcome Foundation
- Chemotherapy Foundation
- March of Dimes
The transcription factor Bcl-6 orchestrates germinal center (GC) reactions through its actions in B cells and T cells and regulates inflammatory signaling in macrophages. Here we found that genetic replacement with mutated Bcl6 encoding Bcl-6 that cannot bind corepressors to its BTB domain resulted in disruption of the formation of GCs and affinity maturation of immunoglobulins due to a defect in the proliferation and survival of B cells. In contrast, loss of function of the BIB domain had no effect on the differentiation and function of follicular helper T cells or that of other helper T cell subsets. Bcl6-null mice had a lethal inflammatory phenotype, whereas mice with a mutant BIB domain had normal healthy lives with no inflammation. The repression of inflammatory responses by Bcl-6 in macrophages was accordingly independent of the repressor function of the BIB domain. Bcl-6 thus mediates its actions through lineage-specific biochemical functions.
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