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IFN‐γ Signaling Is Required to Regulate CD8 T Cell Priming and Development in Contact Sensitivity Responses

Contact hypersensitivity (CHS) is a CD8 T cell mediated immune response to skin sensitization and challenge with hapten. In wild‐type (WT) mice, hapten‐primed CD8 T cell populations producing IFN‐γ and IL‐17 are required for elicitation of CHS. The CHS response to 2,4‐dinitrofluorobenzene (DNFB) was tested in mice lacking the IFN‐γ receptor (IFNγR−/−). CHS responses in senstized IFNγR−/−mice were of similar magnitude to WT mice 24 hr after challenge but were markedly extended in duration. Immunohistology and flow cytometry analyses confirmed increased cellular infiltration into the skin challenge site of IFNγR−/− vs. WT mice through 48 hr post‐challenge. These responses were CD8 T cell dependent as depletion of CD8 T cells abrogated CHS responses in both WT and IFNγR−/−mice. In the skin draining lymph nodes of sensitized WT mice, numbers of hapten‐specific CD8 cells producing IFN‐γ peaked at day 5 post‐sensitization and declined thereafter whereas the numbers of these T cells were elevated at day 5 in IFNγR−/− mice and were sustained through day 8. Depletion of CD8 T cells eliminated the CHS in WT, but not IFNγR−/− ,mice. compared to WT, through 48 hrs. post‐challenge. However, KC production in the skin challenge site is similar in WT and IFNγR−/− mice. Moreover, the numbers of hapten‐specific CD8 T cells producing IL‐17 were 5 fold higher in sensitized IFNγR−/− mice. These results indicate that the absence of IFNγ signaling dysregulates CD8 T cell priming for CHS and increases the development of hapten‐specific CD8 T cells producing IL‐17 which are capable of mediating CHS in the absence of IFN‐γ signaling.