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• W2159976704 endingPage "1560" @default.
• W2159976704 startingPage "1553" @default.
• W2159976704 abstract "To identify defects in B cell tolerance that may contribute to the production of autoantibodies in New Zealand Black (NZB) mice, we crossed soluble hen egg white lysozyme (sHEL) and anti-HEL Ig transgenes (Ig Tg) onto the NZB background. In this study, we have examined one of the first checkpoints involved in maintenance of peripheral B cell tolerance, follicular exclusion and elimination of self-reactive B cells in the absence of T cell help. Freshly isolated anti-HEL Ig Tg B cells were labeled with CFSE, adoptively transferred into sHEL recipients, and the fate of self-reactive anti-HEL Ig Tg B cells was followed using flow cytometry and immunofluorescence microscopy. Although anti-HEL Ig Tg B cells from NZB mice are appropriately excluded from B cell follicles in NZB sHEL recipient mice, they demonstrate aberrant survival, proliferation, and generation of anti-HEL Ab-producing cells. This abnormal response results from an intrinsic defect in NZB B cells, requires the presence of CD4(+) T cells, and is facilitated by the splenic environment in NZB mice. Thus, NZB mice have immune defects that interact synergistically to allow autoreactive B cells to become activated despite the presence of tolerizing autoantigens." @default.
• W2159976704 created "2016-06-24" @default.
• W2159976704 creator A5027872444 @default.
• W2159976704 creator A5042287861 @default.
• W2159976704 creator A5087392266 @default.
• W2159976704 date "2004-02-01" @default.
• W2159976704 modified "2023-09-30" @default.
• W2159976704 title "Autoreactive B Cells in Lupus-Prone New Zealand Black Mice Exhibit Aberrant Survival and Proliferation in the Presence of Self-Antigen In Vivo" @default.
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• W2159976704 doi "https://doi.org/10.4049/jimmunol.172.3.1553" @default.
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