期刊
ELIFE
卷 8, 期 -, 页码 -出版社
ELIFE SCIENCES PUBLICATIONS LTD
DOI: 10.7554/eLife.46997
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资金
- National Institute of Allergy and Infectious Diseases [U19-AI109962, R01-AI117890]
- National Institutes of Health [T32 OD011147, T32 AI060555, 2T32OD010931-09, 5T35OD010956-14]
- National Center for Advancing Translational Sciences [TL1 TR000133]
- German Federal and State Governments Excellence Initiative [EXC 294]
- Deutsche Forschungsgemeinschaft [TRR130-P02]
In mice, neonatally-developing, self-reactive B-1 cells generate steady levels of natural antibodies throughout life. B-1 cells can, however, also rapidly respond to infections with increased local antibody production. The mechanisms regulating these two seemingly very distinct functions are poorly understood, but have been linked to expression of CD5, an inhibitor of BCR-signaling. Here we demonstrate that TLR-mediated activation of CD5+ B-1 cells induced the rapid reorganization of the IgM-BCR complex, leading to the eventual loss of CD5 expression, and a concomitant increase in BCR-downstream signaling, both in vitro and in vivo after infections of mice with influenza virus and Salmonella typhimurium. Both, initial CD5 expression and TLR-mediated stimulation, were required for the differentiation of B-1 cells to IgM-producing plasmablasts after infections. Thus, TLR-mediated signals support participation of B-1 cells in immune defense via BCR-complex reorganization.
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