Abstract：
:Several tolerance checkpoints exist throughout B cell development to control autoreactive B cells and prevent the generation of pathogenic autoantibodies. FcγRIIb 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 FcγRIIb 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 FcγRIIb 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.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Espéli M,Bashford-Rogers R,Sowerby JM,Alouche N,Wong L,Denton AE,Linterman MA,Smith KGCdoi
10.1038/s41467-019-09434-0subject
Has Abstractpub_date
2019-04-29 00:00:00pages
1970issue
1issn
2041-1723pii
10.1038/s41467-019-09434-0journal_volume
10pub_type
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