Interleukin-17 mediated inflammatory responses are required for ultraviolet radiation-induced immune suppression

Academic Article

Abstract

  • © 2014 The American Society of Photobiology. Ultraviolet radiation (UVR) induces immunosuppression and is a major factor for development of skin cancer. Numerous efforts have been made to determine mechanisms for UVR-induced immunosuppression and to develop strategies for prevention and treatment of UVR-induced cancers. In the current study, we use IL-17 receptor (IL-17R) deficient mice to examine whether IL-17 mediated responses have a role in UVB (290-320)-induced immunosuppression of contact hypersensitivity responses. Results demonstrate that IL-17 mediated responses are required for UVB-induced immunosuppression of contact hypersensitivity responses. The systemic immune suppression and development of regulatory T cells are inhibited in UVB-treated IL-17R deficient mice compared to wild-type animals. The deficiency in IL-17R inhibits the infiltration and development of a tolerogenic myeloid cell population in UVB-treated skin, which expresses CD11b and Gr-1 and produces reactive oxygen species. We speculate that the development of the tolerogenic myeloid cells is dependent on IL-17-induced chemokines and inflammatory mediators in UVB-treated skin. The inhibition of the tolerogenic myeloid cells may be attributed to the suppression of regulatory T cells in UVR-treated IL-17R-/- mice. The findings may be exploited to new strategies for prevention and treatment of UVR-induced skin diseases and cancers.
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    Digital Object Identifier (doi)

    Author List

  • Li H; Prasad R; Katiyar SK; Yusuf N; Elmets CA; Xu H
  • Start Page

  • 235
  • End Page

  • 241
  • Volume

  • 91
  • Issue

  • 1