GammadeltaT cells regulate the development of hapten-specific CD8+ effector T cells in contact hypersensitivity responses.
It has been reported that gammadeltaT 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 gammadeltaT cells in the development of contact hypersensitivity, this study employed Tdelta gene knockout mice that are deficient in gammadeltaT cells but are normal in the development of alphabetaT cells. The result indicates that contact hypersensitivity responses were significantly greater in gammadeltaT cell deficient mice than in wild-type mice. Similar results were obtained when wild-type mice were depleted of gammadeltaT cells with antibody treatment before hapten sensitization. Depletion of CD4+ T cells did not affect the increased contact hypersensitivity response in gammadeltaT cell deficient mice, suggesting that the effect of gammadeltaT 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 gammadeltaT cell deficient mice elicited a similar level of contact hypersensitivity in naive wild-type and the deficient recipient mice, indicating that gammadeltaT cells have little effect on the elicitation of primed T cells and contact hypersensitivity responses. We conclude that gammadeltaT 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.
Guan
Hongbing
H
Department of Dermatology, University of Alabama at Birmingham, 1670 University Boulevard, Birmingham, AL 35294, U.S.A.
Zu
Guorui
G
Slater
Marlon
M
Elmets
Craig
C
Xu
Hui
H
D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D018414:CD8-Positive T-Lymphocytes / Q000166:cytology / Q000276:immunology* / Q000378:metabolism; D002478:Cells, Cultured; D003877:Dermatitis, Contact / Q000276:immunology*; D006241:Haptens / Q000276:immunology; D006968:Hypersensitivity, Delayed / Q000276:immunology; D007371:Interferon-gamma / Q000096:biosynthesis; D016753:Interleukin-10 / Q000096:biosynthesis; D015847:Interleukin-4 / Q000096:biosynthesis; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000235:genetics / Q000276:immunology*; D012867:Skin / Q000276:immunology*
D006241:Haptens; D016692:Receptors, Antigen, T-Cell, gamma-delta; D016753:Interleukin-10; D015847:Interleukin-4; D007371:Interferon-gamma