γδT Cells Regulate the Development of Hapten-Specific CD8+ Effector T Cells in Contact Hypersensitivity Responses

It has been reported that γδT cells are required for transfer of contact hypersensitivity responses by hapten-primed T cells. The mechanism by which they do so, however, remains to be elucidated. To specifically investigate the role of γδT cells in the development of contact hypersensitivity, this study employed Tδ gene knockout mice that are deficient in γδT cells but are normal in the development of αβT cells. The result indicates that contact hypersensitivity responses were significantly greater in γδT cell deficient mice than in wild-type mice. Similar results were obtained when wild-type mice were depleted of γδT cells with antibody treatment before hapten sensitization. Depletion of CD4+ T cells did not affect the increased contact hypersensitivity response in γδT cell deficient mice, suggesting that the effect of γδT cells is on CD8+ T cells and does not require CD4+ T cells. Further experiments demonstrated that primed CD8+ T cells from the deficient mice exhibited significantly higher CTL activity. The cytokine profile of CD4+ T cells was not significantly altered. Transfer of primed lymph node cells from hapten-primed γδT cell deficient mice elicited a similar level of contact hypersensitivity in naive wild-type and the deficient recipient mice, indicating that γδT cells have little effect on the elicitation of primed T cells and contact hypersensitivity responses. We conclude that γδT cells downregulate contact hypersensitivity responses to hapten sensitization by limiting the development of hapten-specific CD8+ effector T cells during sensitization and that this effect is independent of CD4+ T cells