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• W1489629488 abstract "Abstract Invariant chain (Ii)-deficient mice exhibit profound B cell defects that have remained poorly understood, because they could not be simply explained by impaired Ag presentation. We found that Ii deficiency induced cell autonomous defects of two distinct B cell lineages. The life span of mature follicular (FO) B cells was reduced, accounting for their markedly decreased frequency, whereas, in contrast, marginal zone (MZ) B cells accumulated. Other Ii-expressing lineages such as B1 B cells and dendritic cells were unaffected. Surprisingly, the life span of FO B cells was fully corrected in Ii/I-Aβ doubly deficient mice, revealing that Ii-free I-Aβ chains alter FO B cell survival. In contrast, the accumulation of MZ B cells was controlled by a separate mechanism independent of I-Aβ. Interestingly, in Ii-deficient mice lacking FO B cells, the MZ B cells invaded the FO zone, suggesting that intact follicules contribute to the retention of B cells in the MZ. These findings reveal unexpected consequences of Ii deficiency on the development and organization of B cell follicles." @default.
• W1489629488 created "2016-06-24" @default.
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• W1489629488 date "2004-02-15" @default.
• W1489629488 modified "2023-09-30" @default.
• W1489629488 title "Mechanisms Governing B Cell Developmental Defects in Invariant Chain-Deficient Mice" @default.
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• W1489629488 doi "https://doi.org/10.4049/jimmunol.172.4.2076" @default.
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