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-Abeta doubly deficient
mice, revealing that Ii-free I-Abeta chains alter FO
B cell survival. In contrast, the accumulation of MZ
B cells was controlled by a separate mechanism independent of I-Abeta. 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.
