Mechanisms Governing B Cell Developmental Defects in Invariant Chain-Deficient Mice

Kamel Benlagha, Se-Ho Park, Rodolphe Guinamard, Claire Forestier, Lars Karlsson, Cheong Hee Chang, Albert Bendelac

Research output: Contribution to journalArticle

16 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)2076-2083
Number of pages8
JournalJournal of Immunology
Volume172
Issue number4
Publication statusPublished - 2004 Feb 15

ASJC Scopus subject areas

  • Immunology

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    Benlagha, K., Park, S-H., Guinamard, R., Forestier, C., Karlsson, L., Chang, C. H., & Bendelac, A. (2004). Mechanisms Governing B Cell Developmental Defects in Invariant Chain-Deficient Mice. Journal of Immunology, 172(4), 2076-2083.