The presence of NK receptors (NKR) on populations of T cells has been proposed to play a regulatory role in T cell function, fine tuning the response to Ag, and influencing the nature of the immune response through rapid secretion of large amounts of cytokines. In this study, we assessed the nature and distribution of NKR on human peripheral blood γδ T cells and established clones to study cytokine release. In circulating γδ T cells, ∼80% expressed CD94, ∼25% expressed NKR-P1A, and ∼20% expressed p58, values substantially higher than those found on αβ T cells from the same donors. When cloned for specific NKR expression, most cells in culture were NKR-P1A+ whereas p58 expression was variable, suggesting that the NKR-P1A phenotype can be acquired in culture whereas expression of p58 is more stable. Some clones were triple positive for CD94, NKR-PIA, and p58. Vδ2+ cells generally expressed a wider range of NKR than Vδ1+ cells. Following activation through CD3, all γδ T cell clones released large amounts of IFN-γ, commencing as early as 4 h postactivation. Some clones also released TNF-α and IL-4, but no correlation with specific NKR expression was noted. Activation through NKR-P1A induced moderate levels of IFN-γ without inducing IL-4. The results suggest that activation of most γδ T cells is regulated by signaling events occurring via both the TCR and the NKR. They further show that peripheral blood γδ T cells may function as a source of the proinflammatory cytokines IFN-γ and TNF-α.
|Number of pages||8|
|Journal||Journal of Immunology|
|Publication status||Published - Oct 15 1997|
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