| First Author | Koni PA | Year | 2001 |
| Journal | J Exp Med | Volume | 193 |
| Issue | 6 | Pages | 741-54 |
| PubMed ID | 11257140 | Mgi Jnum | J:68147 |
| Mgi Id | MGI:1932187 | Doi | 10.1084/jem.193.6.741 |
| Citation | Koni PA, et al. (2001) Conditional Vascular Cell Adhesion Molecule 1 Deletion in Mice. Impaired lymphocyte migration to bone marrow. J Exp Med 193(6):741-54 |
| abstractText | 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. |
