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 language | English |
|---|---|
| Pages (from-to) | 2076-2083 |
| Number of pages | 8 |
| Journal | Journal of Immunology |
| Volume | 172 |
| Issue number | 4 |
| Publication status | Published - 2004 Feb 15 |
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- Immunology
Cite this
Mechanisms Governing B Cell Developmental Defects in Invariant Chain-Deficient Mice. / Benlagha, Kamel; Park, Se-Ho; Guinamard, Rodolphe; Forestier, Claire; Karlsson, Lars; Chang, Cheong Hee; Bendelac, Albert.
In: Journal of Immunology, Vol. 172, No. 4, 15.02.2004, p. 2076-2083.Research output: Contribution to journal › Article
}
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.
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UR - http://www.scopus.com/inward/citedby.url?scp=0842321789&partnerID=8YFLogxK
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 -