| First Author | Dunne JL | Year | 2003 |
| Journal | J Immunol | Volume | 171 |
| Issue | 11 | Pages | 6105-11 |
| PubMed ID | 14634125 | Mgi Jnum | J:100242 |
| Mgi Id | MGI:3588979 | Doi | 10.4049/jimmunol.171.11.6105 |
| Citation | Dunne JL, et al. (2003) Mac-1, but not LFA-1, uses intercellular adhesion molecule-1 to mediate slow leukocyte rolling in TNF-alpha-induced inflammation. J Immunol 171(11):6105-11 |
| abstractText | We have previously shown that Mac-1 and LFA-1 play a cooperative role in slow leukocyte rolling in inflamed vessels, and that, although both have a role in leukocyte adhesion, the contribution from LFA-1 exceeds that of Mac-1. In this study, we used mice deficient in ICAM-1 (ICAM-1(null)) to study the function of ICAM-1 as an endothelial ligand for Mac-1 and LFA-1. The cremaster muscles of these mice were treated with TNF-alpha and prepared for intravital microscopy. We found that the average rolling velocity in venules was not different in ICAM-1(null) mice (4.7 micro m/s) compared with wild-type mice (5.1 micro m/s). Similarly, leukocyte adhesion efficiency in ICAM-1(null) mice (0.11 +/- 0.01 mm) was similar to that in Mac-1(-/-) (0.12 +/- 0.03 mm) mice but significantly increased compared with that in LFA-1(-/-) (0.08 +/- 0.01 mm) mice and significantly reduced from that in wild type (0.26 +/- 0.04 mm). When both LFA-1 and ICAM-1 were blocked, rolling velocity increased, and adhesion efficiency and arrest decreased. However, blocking both Mac-1 and ICAM-1 had no greater effect than either blockade alone. We conclude that endothelial ICAM-1 is the main ligand responsible for slow leukocyte rolling mediated by Mac-1, but not LFA-1. |
