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Different HLA class I-specific killer inhibitory receptors (KIR) are expressed in vivo by a fraction of activated T cells, predominantly CD8+, in which they may inhibit TCR-mediated cell functions. In an attempt to identify mechanisms leading to KIR expression in T cells, we analyzed the effect of transforming growth factor-beta (TGF-beta) in T cells responding to bacterial superantigens in vitro. We show that TGF-beta induces the expression of CD94/NKG2A in cells responding to toxic shock syndrome toxin 1 or to other staphylococcal superantigens. Remarkably, maximal CD94 expression occurred at (low) TGF-beta concentrations which have no substantial effect on lymphocyte proliferation. Maximal CD94 expression occurred when TGF-beta was added shortly after the cells were placed in culture. No expression could be induced in CD94/NKG2A-negative T cell clones. Although both CD4+ and CD8+ expressed CD94, the simultaneous expression of NKG2A was mostly confined to CD8+ cells. Monoclonal antibody-mediated cross-linking of CD94/NKG2A led to an impairment of T cell triggering via CD3, as determined in a redirected killing assay using the Fcgamma receptor-positive P815 murine target cells.
Bertone et al. (Fri,) studied this question.