Vascular cellular adhesion molecule (VCAM)-1 is a membrane-bound cellular adhesion molecule that mediates adhesive interactions between hematopoietic progenitor cells and stromal cells in the bone marrow (BM) and between leukocytes and endothelial as well as dendritic cells. Since VCAM-1–deficient mice die embryonically, conditional VCAM-1 mutant mice were generated to analyze the in vivo function of this adhesion molecule. Here we show that interferon-induced Cre-loxP–mediated deletion of the VCAM-1 gene after birth efficiently ablates expression of VCAM-1 in most tissues like, for example, BM, lymphoid organs, and lung, but not in brain. Induced VCAM-1 deficiency leads to a reduction of immature B cells in the BM and to an increase of these cells in peripheral blood but not in lymphoid organs. Mature recirculating B cells are reduced in the BM. In a migration assay, the number of mature B cells that appears in the BM after intravenous injection is decreased. In addition, the humoral immune response to a T cell–dependent antigen is impaired. VCAM-1 serves an important role for B cell localization and the T cell–dependent humoral immune response.
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19 March 2001
Article|
March 19 2001
Neonatally Induced Inactivation of the Vascular Cell Adhesion Molecule 1 Gene Impairs B Cell Localization and T Cell–Dependent Humoral Immune Response
Christoph E. Leuker,
Christoph E. Leuker
aInstitute for Genetics, University of Cologne, D-50931 Cologne, Germany
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Mark Labow,
Mark Labow
bDepartment of Functional Genomics, Novartis Pharmaceuticals, Incorporated, Summit, New Jersey 07901
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Werner Müller,
Werner Müller
aInstitute for Genetics, University of Cologne, D-50931 Cologne, Germany
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Norbert Wagner
Norbert Wagner
aInstitute for Genetics, University of Cologne, D-50931 Cologne, Germany
cDepartment of Pediatrics, University of Bonn, D-53113 Bonn, Germany
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Christoph E. Leuker
aInstitute for Genetics, University of Cologne, D-50931 Cologne, Germany
Mark Labow
bDepartment of Functional Genomics, Novartis Pharmaceuticals, Incorporated, Summit, New Jersey 07901
Werner Müller
aInstitute for Genetics, University of Cologne, D-50931 Cologne, Germany
Norbert Wagner
aInstitute for Genetics, University of Cologne, D-50931 Cologne, Germany
cDepartment of Pediatrics, University of Bonn, D-53113 Bonn, Germany
Abbreviations used in this paper: APC, allophycocyanin; BM, bone marrow; BrdU, bromodeoxyuridine; CXCR, CXC chemokine receptor; HPC, hematopoietic progenitor cell; HSA, heat stable antigen; ICAM, intercellular adhesion molecule; NP-CG, (4-hydroxy-3-nitrophenyl)-acetyl-chicken globulin; VCAM, vascular cell adhesion molecule; VLA, very late antigen.
Received:
July 18 2000
Revision Requested:
February 13 2001
Accepted:
February 13 2001
Online ISSN: 1540-9538
Print ISSN: 0022-1007
© 2001 The Rockefeller University Press
2001
The Rockefeller University Press
J Exp Med (2001) 193 (6): 755–768.
Article history
Received:
July 18 2000
Revision Requested:
February 13 2001
Accepted:
February 13 2001
Citation
Christoph E. Leuker, Mark Labow, Werner Müller, Norbert Wagner; Neonatally Induced Inactivation of the Vascular Cell Adhesion Molecule 1 Gene Impairs B Cell Localization and T Cell–Dependent Humoral Immune Response. J Exp Med 19 March 2001; 193 (6): 755–768. doi: https://doi.org/10.1084/jem.193.6.755
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