期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 118, 期 8, 页码 2896-2907出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI35618
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资金
- NIAID NIH HHS [P01 AI51392, P01 AI051392] Funding Source: Medline
- NIAMS NIH HHS [R37 AR032371] Funding Source: Medline
- PHS HHS [R37 ARO 32371] Funding Source: Medline
Autoreactive B cells are regulated in the BM during development through mechanisms, including editing of the B cell receptor (BCR), clonal deletion, and anergy. Peripheral B cell tolerance is also important for protection from autoimmune damage, although the mechanisms are less well defined. Here we demonstrated, using a mouse model of SLE-like serology, that during an autoimmune response, RAG was reinduced in antigen-activated early memory or preplasma B cells. Expression of RAG was specific to antigen-reactive B cells, required the function of the IL-7 receptor (IL-7R), and contributed to maintenance of humoral tolerance. We also showed that soluble antigen could diminish a non-autoreactive antibody response through induction of BCR revision. These data suggest that tolerance induction operates in B cells at a postactivation checkpoint and that BCR revision helps regulate autoreactivity generated during an ongoing immune response.
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