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International Immunology, Vol. 14, No. 7, pp. 751-760, July 2002
© 2002 Japanese Society for Immunology

Differential role of E-selectin and P-selectin in T lymphocyte migration to cutaneous inflammatory reactions induced by cytokines

Anna A. Kulidjian1, Andrew C. Issekutz2 and Thomas B. Issekutz2

1 Department of Immunology, University of Toronto, Toronto, Ontario M5S 1A8, Canada 2 Departments of Pediatrics, Microbiology/Immunology and Pathology, Dalhousie University, Halifax, Nova Scotia B3J 3G9, Canada

Correspondence to: T. B. Issekutz, 8 East Research, IWK Health Centre, 5850 University Avenue, Halifax, Nova Scotia B3J 3G9, Canada. E-mail: Thomas.Issekutz{at}.dal.ca
Transmitting editor: M. Miyasaka

E-selectin and P-selectin are thought to be important in the infiltration of T lymphocytes in inflammation, but their role in cytokine-induced cutaneous inflammatory reactions has not been examined. A technique for quantifying labeled T lymphocyte migration to cytokine-induced dermal inflammation in mice was developed. After i.v. injection, 51Cr-labeled T lymphocytes migrated to lesions induced by IFN-{gamma} and tumor necrosis factor (TNF)-{alpha}, and in even greater numbers to the combination of IFN-{gamma} + TNF-{alpha}, and to sites injected with concanavalin A (Con A). In E-selectin mAb-treated and in E-selectin-deficient mice, IFN-{gamma}-, IFN-{gamma} + TNF-{alpha}- and Con A-induced T cell accumulation was inhibited by 45–65%, but TNF-{alpha}-induced infiltration was unaffected. In P-selectin mAb-treated and P-selectin-deficient mice, T cell accumulation remained unchanged in most of the lesions. Combined, E-selectin and P-selectin mAb treatment inhibited T cell accumulation in all four types of reactions, and significantly more than E-selectin blockade alone in migration to Con A. Results in E-selectin- and P-selectin-deficient mice confirmed these observations, and demonstrated strain-dependent differences in the contributions of the two selectins. In conclusion, T cells migrating to dermal inflammatory reactions utilize both E-selectin and P-selectin, but alternate adhesion pathways also contribute, since blocking both endothelial selectins does not abolish T cell migration. P-selectin plays a less important role than E-selectin, since blocking E-selectin, but not P-selectin, alone decreased T cell accumulation. The relative contribution of the selectins varies depending on the initiating inflammatory stimulus and the genetic background.

Keywords: adhesion molecule, delayed-type hypersensitivity, in vivo animal model, inflammation, recruitment


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