TCR$\alpha\beta$+ CD8+ and TCR$\gamma\delta$+ lymphocytes inhibit the capability of peritoneal macrophages to induce contact hypersensitivity

Macrophages (Mf) play an important role in induction and regulation of the immune response. It was shown previously that subcutaneous injection of hapten conjugated macrophages (TNP-Mf) induces the contact hypersensitivity (CHS) response, whereas intravenous (i.v.) or intraperitioneal administration of TNP-Mf results in unresponsiveness as a result of induced T suppressor (Ts) cells. The aim of this study was to determine if different T cell populations influence macrophages to become inducers of immunological suppression. Our findings show that indeed i.v. injection of TNP labeled macrophages isolated from control mice into syngenic recipients induces unresponsiveness. However, i.v. administration of TNP substituted macrophages isolated from TCR\alpha-/-, TCR\delta-/- and \beta_{2}m-/- mice induces strong CHS similar to that observed after skin painting with TNP-Cl. Moreover, it was shown that TNP conjugated macrophages isolated from CD1d-/- mice were still able to promote immunosuppression when injected intravenously. This suggests that TCR\alpha\beta+ CD8+ and TCR\gamma\delta+ lymphocytes stimulate macrophages to induce immunosuppression instead of a strong CHS reaction, whereas CD1d dependent NKT cells are not involved in negative regulation of macrophage function.