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* Department of Pathology, University of Chicago, Chicago, IL 60637;
Department of Biology, BK21 Graduate School of Biotechnology, Korea University, Seoul, South Korea;
Centre d’Immunologie de Marseille Luminy, Centre National de la Recherche Scientifique-Institut National de la Santé et de la Recherche Médicale-Universite de la Mediterrannee, Parc Scientifique de Luminy, Marseille, France;
R. W. Johnson Pharmaceutical Research Institute, San Diego, CA 92121; and
¶
Department of Microbiology and Immunology, Walter Oncology Center, Indiana University School of Medicine, Indianapolis, IN 46202
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-A
doubly deficient mice, revealing that Ii-free I-A chains alter FO B cell survival. In contrast, the accumulation of MZ B cells was controlled by a separate mechanism independent of I-A. 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.
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