Specific superantigens activate different T-cell fractions with distinct TCR Vβ elements in association with MHC class II molecules and also induce SDCC against MHC class II+ target cells. In the present study, to determine whether the responsiveness of each CD8 + T-cell fraction expressing a different TCR Vβ element is primarily determined by the TCR Vβ, we compared the levels of proliferation and SDCC in Vβ3
List of Abbreviations:AC, accessory cells; CFSE, five-(and 6) carboxyfluorescein diacetate succinimidyl ester; FCS, fetal calf serum; FITC, fluoresceinisothiocyanate; MHC, major histocompatibility complex; SAG, superantigens; SEA, staphylococcal enterotoxin A; SDCC, SAG-dependent cell-mediated cytotoxicity; SEA m , mutant SEA; SEA wt , wild-type SEA; TCR, T-cell receptor; TSS, toxic shock syndrome.the TCR Vβ irrespective of the CD4/CD8 T-cell subset. Our previous study using mini-osmotic pumps filled with SEA (7) showed that the SEA-induced response tended to be stronger in the Vβ3 + CD4 + T-cell fraction than in the Vβ11 + CD4 + T-cell fraction. Using this system, only a transient expansion was induced in SEA-reactive CD8 + T cells, and different responses among the SEA-reactive CD8 + T-cell subpopulations expressing different TCR Vβ elements were not observed. SAG can also induce human and murine CD4 + and CD8 + T cells to kill MHC class II +