Expression of type 3 complement receptor on activated CD8+ T cells facilitates homing to inflammatory sites.

It has been reported that Ag-primed T cells may express the type 3 complement receptor (CR3; CD11b/CD18, Mac-1), but no clear function has been ascribed to this molecule on T cells. In our study, we have used a nondepleting mAb to CR3 (5C6) to study the relevance of CR3 expression for T-cell extravasation at inflammatory foci. The in vivo administration of 5C6 significantly reduced the severity of the T cell-mediated meningitis induced by intracerebral inoculation of lymphocytic choriomeningitis virus. FACS analysis of the inflammatory exudate showed that this consists of monocytes/macrophages and CD8+ cells, the majority of which are CD11b+. Adoptive transfer experiments involving i.v. transplantation of Ag-primed donor cells revealed that preincubation of the cells with 5C6 delayed the virus-specific delayed-type hypersensitivity reaction under conditions in which the recipient delivered the nonspecific component. In contrast, preincubation with 5C6 did not inhibit the response when donor cells were injected locally. The reaction induced by locally injected, adherent cell-depleted donor cells was, on the other hand, delayed by i.v. injection of 5C6 to the recipient. These results indicate that anti-CR3 treatment inhibits extravasation of both the Ag-specific and the nonspecific cellular components of the lymphocytic choriomeningitis virus-induced, CD8+ cell-dependent inflammatory reaction. Thus, expression of CR3 seems to facilitate T cell homing to sites of inflammation.