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Brief Definitive Report |
Correspondence to: Bruce Furie, Research East #319/Beth Israel Deaconess Medical Center, Boston, MA 02215. Tel:617-667-0620 Fax:617-975-5505 E-mail:bfurie{at}caregroup.harvard.edu.
P-selectin glycoprotein ligand 1 (PSGL-1) is a sialomucin expressed on leukocytes that mediates neutrophil rolling on the vascular endothelium. Here, the role of PSGL-1 in mediating lymphocyte migration was studied using mice lacking PSGL-1. In a contact hypersensitivity model, the infiltration of CD4+ T lymphocytes into the inflamed skin was reduced in PSGL-1–deficient mice. In vitro–generated T helper (Th)1 cells from PSGL-1–deficient mice did not bind to P-selectin and migrated less efficiently into the inflamed skin than wild-type Th1 cells. To assess the role of PSGL-1 in P- or E-selectin–mediated migration of Th1 cells, the cells were injected into E- or P-selectin–deficient mice. PSGL-1–deficient Th1 cells did not migrate into the inflamed skin of E-selectin–deficient mice, indicating that PSGL-1 on Th1 cells is the sole ligand for P-selectin in vivo. In contrast, PSGL-1–deficient Th1 cells migrated into the inflamed skin of P-selectin–deficient mice, although less efficiently than wild-type Th1 cells. This E-selectin–mediated migration of PSGL-1–deficient or wild-type Th1 cells was not altered by injecting a blocking antibody to L-selectin. These data provide evidence that PSGL-1 on Th1 cells functions as one of the E-selectin ligands in vivo.
Key Words: cellular immunity, contact hypersensitivity, P-selectin, E-selectin, knockout mice
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