Activation of human T cells with NK cell markers by staphylococcal enterotoxin A via IL-12 but not via IL-18

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Abstract
We have reported recently that mouse liver NK cells and NK1·1+ T cells were activated by bacterial superantigens via the IL‐12 production from Kupffer cells. In the present study, we examined the effect of staphyloccoccal enterotoxin A (SEA) on human T cells with NK cell markers, CD56 or CD57 (NK‐type T cells). After stimulating peripheral blood mononuclear cells (PBMC) with SEA, PBMC produced a large amount of IFN‐γ and acquired a potent antitumour cytotoxicity. The in vitro depletion of either CD56+ TCR– NK cells, CD56+ T cells or 57+ T cells from PBMC significantly inhibited the IFN‐γ production from PBMC. When purified NK‐type T cells, NK cells and regular T cells were cultured with monocytes and SEA they all produced IFN‐γ, while the IFN‐γ amounts produced by both NK‐type T cells were greater than those produced by NK cells. NK cells as well as CD56+ T cells showed cytotoxicity against NK‐sensitive K562 cells, whereas both NK‐type T cells showed a more potent cytotoxicity against NK‐resistant Raji cells than did NK cells. The IFN‐γ production from each population as well as from whole PBMC was greatly inhibited by anti‐IL‐12 antibody but not by anti‐IL‐18 antibody. The antitumour cytotoxicity of whole PBMC was also significantly inhibited by anti‐IL‐12 antibody while the SEA‐induced proliferation of PBMC was not affected by anti‐IL‐12 antibody. Furthermore, SEA‐activated NK‐type T cells as well as NK cells showed cytotoxicities against vascular endothelial cells. Our findings suggest that human NK‐type T cells are thus involved in bacterial superantigen‐induced immune response.

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