TY - JOUR
T1 - Mechanisms Governing B Cell Developmental Defects in Invariant Chain-Deficient Mice
AU - Benlagha, Kamel
AU - Park, Se Ho
AU - Guinamard, Rodolphe
AU - Forestier, Claire
AU - Karlsson, Lars
AU - Chang, Cheong Hee
AU - Bendelac, Albert
PY - 2004/2/15
Y1 - 2004/2/15
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=0842321789&partnerID=8YFLogxK
U2 - 10.4049/jimmunol.172.4.2076
DO - 10.4049/jimmunol.172.4.2076
M3 - Article
C2 - 14764672
AN - SCOPUS:0842321789
VL - 172
SP - 2076
EP - 2083
JO - Journal of Immunology
JF - Journal of Immunology
SN - 0022-1767
IS - 4
ER -