期刊
JOURNAL OF IMMUNOLOGY
卷 179, 期 11, 页码 7544-7552出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.179.11.7544
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资金
- Intramural NIH HHS Funding Source: Medline
- NIAID NIH HHS [AI29576, AI43587] Funding Source: Medline
Ligation of B cell receptors on immature bone marrow B cells, either by an endogenous Ag or by an anti-B cell receptor Ab induces secondary V(D)J gene rearrangements, termed receptor editing. Whether the same signal induces receptor editing in transitional B cells is not clear. In this study, we examined the responses of immature and transitional B cells from V(H)12V kappa 1A Ig transgenic mice to stimulation with an anti-Ig beta Ab. Our results demonstrated that immature B cells stimulated with a low concentration of anti-Ig beta Ab, mimicking Ag stimulation, underwent receptor editing both in vivo and in vitro, as evidenced by the detection of dsDNA breaks at J kappa recombination signal sequences, whereas transitional B cells did not. The lack of dsDNA breaks in transitional B cells contrasts with their increased expression of RAG1 and RAG2, suggesting a novel mechanism that may prevent rearrangements. Furthermore, treatment of transitional B cells with high concentrations of anti-Ig beta Abs induced apoptosis, whereas low concentrations induced differentiation. Our results support the idea that transitional B cells lose the capacity to edit, but are sensitive to positive and negative selection.
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