IL-17 and IFN-gamma mediate the elicitation of contact hypersensitivity responses by different mechanisms and both are required for optimal responses.

ABSTRACT: Hapten-induced contact hypersensitivity (CHS) in the skin is a delayed type cellular immune response that can be mediated by CD8(+) T cells that produce IFN-gamma or IL-17. However, mechanisms for these cytokines in the elicitation of CHS remain to be fully elucidated. In this study, we show that adoptive transfer of CHS with hapten-primed wild-type (WT) CD8(+) T cells is reduced in IFN-gammaR(-/-) or IL-17R(-/-) mice compared with WT controls. The infiltration of granulocytes and macrophages in the hapten challenged skin of IL-17R(-/-) recipients is significantly reduced whereas it is less affected in IFN-gammaR(-/-) recipients although CD8(+) T cell infiltration is inhibited in both recipients. In contrast, the activity of reactive oxidative species is significantly inhibited in IFN-gamm

SUBMITTER: He D 

PROVIDER: S-EPMC3179907 | biostudies-literature | 2009 Jul

REPOSITORIES: biostudies-literature