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Original Article

Pandelakis A. Koni^a, Sunil K. Joshi^a, Ulla-Angela Temann^b, Dian Olson^d, Linda Burkly^d, and Richard A. Flavell^b,c

^a Molecular Immunology Program, Institute of Molecular Medicine and Genetics, and Department of Medicine, Medical College of Georgia, Augusta, Georgia 30912
^b Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520
^c Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut 06520
^d Biogen Incorporated, Boston, Massachusetts 02142
Rm. CA2007, Institute of Molecular Medicine and Genetics, Medical College of Georgia, 1120 15 St., Augusta, GA 30912.706-721-7959706-721-6897

lak{at}immag.mcg.edu

We generated vascular cell adhesion molecule (VCAM)-1 "knock-in" mice and Cre recombinase transgenic mice to delete the VCAM-1 gene (vcam-1) in whole mice, thereby overcoming the embryonic lethality seen with conventional vcam-1–deficient mice. vcam-1 knock-in mice expressed normal levels of VCAM-1 but showed loss of VCAM-1 on endothelial and hematopoietic cells when interbred with a "TIE2Cre" transgene. Analysis of peripheral blood from conditional vcam-1–deficient mice revealed mild leukocytosis, including elevated immature B cell numbers. Conversely, the bone marrow (BM) had reduced immature B cell numbers, but normal numbers of pro-B cells. vcam-1–deficient mice also had reduced mature IgD⁺ B and T cells in BM and a greatly reduced capacity to support short-term migration of transferred B cells, CD4⁺ T cells, CD8⁺ T cells, and preactivated CD4⁺ T cells to the BM. Thus, we report an until now unappreciated dominant role for VCAM-1 in lymphocyte homing to BM.

Key Words: VCAM-1 • Cre recombinase • knockout mice • bone marrow • lymphocyte migration

Abbreviations used in this paper: BM, bone marrow; CG, chicken -globulin; CMFDA, 5-chloromethylfluorescein diacetate; DC, dendritic cell; EC, endothelial cell; ES, embryonic stem; FDC, follicular dendritic cell; GC, germinal center; HEV, high endothelial venule; ICAM, intercellular adhesion molecule; MLN, mesenteric LN; NP, 4-hydroxy-3-nitrophenyl; PLN, peripheral LN; PNA, peanut agglutinin; VCAM, vascular cell adhesion molecule; VLA, very late antigen.

© 2001 The Rockefeller University Press

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• Dansky, H. M., Barlow, C. B., Lominska, C., Sikes, J. L., Kao, C., Weinsaft, J., Cybulsky, M. I., Smith, J. D. (2001). Adhesion of Monocytes to Arterial Endothelium and Initiation of Atherosclerosis Are Critically Dependent on Vascular Cell Adhesion Molecule-1 Gene Dosage. Arterioscler. Thromb. Vasc. Bio. 21: 1662-1667 [Abstract] [Full Text]  
• Fortin, A., Cardon, L. R., Tam, M., Skamene, E., Stevenson, M. M., Gros, P. (2001). Identification of a malaria new susceptibility locus (Char4) in recombinant congenic strains of mice. Proc. Natl. Acad. Sci. USA 10.1073/pnas.191288998v1 [Abstract] [Full Text]  
• Bouvard, D., Brakebusch, C., Gustafsson, E., Aszodi, A., Bengtsson, T., Berna, A., Fassler, R. (2001). Functional Consequences of Integrin Gene Mutations in Mice. Circ. Res. 89: 211-223 [Abstract] [Full Text]  
• Hargreaves, D. C., Hyman, P. L., Lu, T. T., Ngo, V. N., Bidgol, A., Suzuki, G., Zou, Y.-R., Littman, D. R., Cyster, J. G. (2001). A Coordinated Change in Chemokine Responsiveness Guides Plasma Cell Movements. JEM 194: 45-56 [Abstract] [Full Text]  
• Leuker, C. E., Labow, M., Muller, W., Wagner, N. (2001). Neonatally Induced Inactivation of the Vascular Cell Adhesion Molecule 1 Gene Impairs B Cell Localization and T Cell-Dependent Humoral Immune Response. JEM 193: 755-768 [Abstract] [Full Text]  
• Fortin, A., Cardon, L. R., Tam, M., Skamene, E., Stevenson, M. M., Gros, P. (2001). Identification of a new malaria susceptibility locus (Char4) in recombinant congenic strains of mice. Proc. Natl. Acad. Sci. USA 98: 10793-10798 [Abstract] [Full Text]  

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