| First Author | Venturi GM | Year | 2003 |
| Journal | Immunity | Volume | 19 |
| Issue | 5 | Pages | 713-24 |
| PubMed ID | 14614858 | Mgi Jnum | J:142184 |
| Mgi Id | MGI:3820521 | Doi | 10.1016/s1074-7613(03)00295-4 |
| Citation | Venturi GM, et al. (2003) Leukocyte migration is regulated by L-selectin endoproteolytic release. Immunity 19(5):713-24 |
| abstractText | L-selectin mediates lymphocyte migration to peripheral lymph nodes and leukocyte rolling on vascular endothelium during inflammation. One unique feature that distinguishes L-selectin from other adhesion molecules is that it is rapidly cleaved from the cell surface after cellular activation. The biological significance of L-selectin endoproteolytic release was determined by generating gene-targeted mice expressing a modified receptor that was not cleaved from the cell surface. Blocking L-selectin cleavage on antigen-stimulated lymphocytes allowed their continued migration to peripheral lymph nodes and inhibited their short-term redirection to the spleen. Blocking homeostatic L-selectin cleavage also resulted in a constitutive 2-fold increase in overall L-selectin expression by leukocytes. As a result, neutrophils entered the inflamed peritoneum in greater numbers or for a longer duration. Thus, endoproteolytic cleavage regulates both homeostatic and activation-induced changes in cell surface L-selectin density, which directs the migration patterns of activated lymphocytes and neutrophils in vivo. |
