Cultured Kaposi's Sarcoma Tumor Cells Fail to Stimulate T Cell Proliferation

Abstract

Prior to the AIDS epidemic, Kaposi's sarcoma (KS) was a rare neoplasm. However, in the context of immunosuppression, cutaneous KS lesions more frequently develop and express various surface molecules recognized by T cells such as intercellular adhesion molecule-1 (ICAM-1; CD54) and HLA–DR. The KS tumor cells are thought to arise locally from endothelial cells via a transdifferentiation process. To determine if KS tumor 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-activated endothelial cells, which were induced to express B7-1, but not B7-2 and could function in bacteria-derived superantigen-driven T cell proliferation, four different KS tumor cell lines failed to express either B7-1 or B7-2 and were unable to stimulate allogeneic T cell proliferation upon addition of bacteria-derived superantigen. These results suggest that KS tumor cells behave differently in their response to cytokines compared with endothelial cells and may be able to evade the local immune response by not expressing costimulatory molecules necessary for T cell proliferation.