期刊
NATURE COMMUNICATIONS
卷 10, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41467-019-09434-0
关键词
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资金
- Cambridge NIHR BRC Cell Phenotyping Hub
- Wellcome Trust [200871/Z/16/Z, WT106068AIA, 083650/Z/07/Z]
- NIHR Cambridge Biomedical Research Centre
- Laboratory of Excellence in Research on Medication and Innovative Therapeutics (LabEx LERMIT) - ANR [ANR-10-LABX-33, ANR-11-IDEX-0003-01]
- ANR@RAction starting grant [ANR-14-ACHN-0008]
- BBSRC [BBS/E/B/000C0427, BBS/E/B/000C0407] Funding Source: UKRI
- Agence Nationale de la Recherche (ANR) [ANR-14-ACHN-0008] Funding Source: Agence Nationale de la Recherche (ANR)
Several tolerance checkpoints exist throughout B cell development to control autoreactive B cells and prevent the generation of pathogenic autoantibodies. Fc gamma RIIb is an Fc receptor that inhibits B cell activation and, if defective, is associated with autoimmune disease, yet its impact on specific B cell tolerance checkpoints is unknown. Here we show that reduced expression of Fc gamma RIIb enhances the deletion and anergy of autoreactive immature B cells, but in contrast promotes autoreactive B cell expansion in the germinal center and serum autoantibody production, even in response to exogenous, non-self antigens. Our data thus show that Fc gamma RIIb has opposing effects on pre-immune and post-immune tolerance checkpoints, and suggest that B cell tolerance requires the control of bystander germinal center B cells with low or no affinity for the immunizing antigen.
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