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

Fingerprint

B-Lymphocytes
invariant chain
Cell Lineage
Dendritic Cells
Cell Survival

ASJC Scopus subject areas

  • Immunology

Cite this

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.

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 journalArticle

Benlagha, K, Park, S-H, Guinamard, R, Forestier, C, Karlsson, L, Chang, CH & Bendelac, A 2004, 'Mechanisms Governing B Cell Developmental Defects in Invariant Chain-Deficient Mice', Journal of Immunology, vol. 172, no. 4, pp. 2076-2083.
Benlagha K, Park S-H, Guinamard R, Forestier C, Karlsson L, Chang CH et al. Mechanisms Governing B Cell Developmental Defects in Invariant Chain-Deficient Mice. Journal of Immunology. 2004 Feb 15;172(4):2076-2083.
Benlagha, Kamel ; Park, Se-Ho ; Guinamard, Rodolphe ; Forestier, Claire ; Karlsson, Lars ; Chang, Cheong Hee ; Bendelac, Albert. / Mechanisms Governing B Cell Developmental Defects in Invariant Chain-Deficient Mice. In: Journal of Immunology. 2004 ; Vol. 172, No. 4. pp. 2076-2083.
@article{4a6400c792a34b3c8db6dccd3cc600ea,
title = "Mechanisms Governing B Cell Developmental Defects in Invariant Chain-Deficient Mice",
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.",
author = "Kamel Benlagha and Se-Ho Park and Rodolphe Guinamard and Claire Forestier and Lars Karlsson and Chang, {Cheong Hee} and Albert Bendelac",
year = "2004",
month = "2",
day = "15",
language = "English",
volume = "172",
pages = "2076--2083",
journal = "Journal of Immunology",
issn = "0022-1767",
publisher = "American Association of Immunologists",
number = "4",

}

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

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 -