CULTURED KAPOSIS-SARCOMA TUMOR-CELLS FAIL TO STIMULATE T-CELL PROLIFERATION

Prior to the AIDS epidemic, Kaposi's sarcoma (KS) was a rare neoplasm, However, in the context of immunosuppression, cutaneous KS lesions mo re frequently develop and express various surface molecules recognized by T cells such as intercellular adhesion molecule-1 (ICAM-1; CD54) a nd HLA-DR. The KS tumor cells are thought to arise locally from endoth elial cells via a transdifferentiation process. To determine if KS tum or cells can stimulate resting T cell proliferation, we asked whether the tumor cells express the critically important T cell costimulatory molecules B7-1 (CD80) and B7-2 (CD86), In contrast to cytokine-activat ed endothelial cells, which were induced to express B7-1, but not B7-2 and could function in bacteria-derived superantigen-driven T cell pro liferation, four different KS tumor cell lines failed to express eithe r B7-1 or B7-2 and were unable to stimulate allogeneic T cell prolifer ation upon addition of bacteria-derived superantigen. These results su ggest that KS tumor cells behave differently in their response to cyto kines compared with endothelial cells and may be able to evade the loc al immune response by not expressing costimulatory molecules necessary for T cell proliferation. (C) 1996 Academic Press, Inc.