MHC class II-dependent activation of CD4(+) T cell hybridomas by human mast cells through superantigen presentation

Human mast cells (MC) were examined for expression of MHC class II antigens and for their ability to activate CD4(+) T cell hybridomas through present ation of superantigen (SAg), HMC-1, a leukemic immature MC line expressing class II Ags, was shown to efficiently present the staphylococcal enterotox in B (SEB) SAg to responding T cell hybridoma on treatment with interferon- gamma (IFN-gamma), which up-regulated class II molecules. The study was the n extended to human normal MC. Almost pure (>99%) cord blood-derived MC (CB MC) were shown to express class II Ags (HLA-DR and HLA-DQ) and CD80, which were upregulated by IFN-gamma treatment and, to a lesser extent, by interle ukin-4 (IL-4) and granulocyte-macrophage colony-stimulating factor (GM-CSF) . CBMC directly activated CD4(+) T cell hybridomas through presentation of SEE and TSST1 SAgs, The production of IL-2 required a cell-to-cell contact between T cells and CBMC and it was inhibited by anti-class II antibodies. Furthermore, an additional pretreatment of CBMC by IFN-gamma or GM-CSF or I L-4 had no effect on their presenting efficiency. This previously unknown f unction of human MC, i.e., MHC class II-dependent activation of CD4(+) T ce lls, may be critical in subsequent cellular activation events because coloc alization of mast and T cells is frequently observed at sites of antigen en try.