| First Author | Schenkel AR | Year | 2004 |
| Journal | J Immunol | Volume | 173 |
| Issue | 10 | Pages | 6403-8 |
| PubMed ID | 15528380 | Mgi Jnum | J:94283 |
| Mgi Id | MGI:3511740 | Doi | 10.4049/jimmunol.173.10.6403 |
| Citation | Schenkel AR, et al. (2004) Platelet endothelial cell adhesion molecule deficiency or blockade significantly reduces leukocyte emigration in a majority of mouse strains. J Immunol 173(10):6403-8 |
| abstractText | PECAM is a molecule used specifically during the diapedesis step when neutrophils and monocytes leave the blood compartment. Anti-PECAM reagents, such as Abs and soluble fusion proteins, block diapedesis both in vivo and in vitro. However, the PECAM knockout mouse in C57BL/6 strain has no serious defects in most models of inflammation. We show in this study that the same PECAM knockout backcrossed into the FVB/n strain clearly has reduced leukocyte emigration in two models of inflammation. Furthermore, we show that anti-PECAM reagents can block leukocyte emigration in several other wild-type strains of mice like FVB/n, SJL, and the outbred strain Swiss Webster. This clearly shows that the C57BL/6 strain is uniquely able to compensate for the loss of PECAM function. Murine models of inflammatory disease that have been studied using C57BL/6 mice should be re-evaluated using FVB/n or other mouse strains to determine whether PECAM plays a role in those models. |
