T-Cell-Dependent And T-Cell-Independent Stimulation Of Hamster Spleen Nk-Like Cells With Concanavalin-A

This study was designed to examine the inducibility and lineage of nonspecifically cytotoxic effector cells in the hamster spleen. Employing a known T cell mitogen, concanavalin A (ConA), and a monoclonal antibody against a recently identified hamster T cell marker (Thy 1.2 homologue), we examined the effector cells induced in spleen by ConA and the role of T cells in regulating this response. Cytotoxicity was measured against uninfected baby hamster kidney cells, cells infected with herpes simplex virus, or a mouse target, SV3T3, in a 16-hr 51Cr release assay. Pretreatment of spleen cells with ConA (2.5-10 micrograms ConA/ml) markedly augmented killing of all targets. Although ConA pretreatment of effector cells enhanced cytotoxicity, pretreatment of targets did not, indicating that ConA is acting at the effector cell level. Supernatants from ConA-stimulated spleen cells also augmented spleen lymphocyte cytotoxicity, suggesting that the ConA effect is mediated by lymphokines (LK). Depletion of Thy 1.2-positive cells from the spleen cells failed to influence augmentation of cytotoxicity by either ConA or ConA-induced LK, indicating that the precursor cells are not T cells. However, depletion of Thy 1.2-positive cells completely eliminated the production of LK in response to ConA, indicating that the factors in LK that augment cytotoxicity are strictly T cell dependent. Whether nonspecific cytotoxic cells induced by ConA in the absence of T cells and by the T cell LK are the same population is not known. None of the cytotoxicity induced from intact or T cell-depleted spleen cells by either ConA or LK expressed the Thy 1.2 homologue. These results suggest that nonspecific cytotoxic lymphocytes of non-T cell lineage in the hamster are regulated via both T cell-dependent and T cell-independent mechanisms.