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Interleukin‐17 Mediated Inflammatory Responses Are Required for Ultraviolet Radiation‐Induced Immune Suppression
Author(s) -
Li Hui,
Prasad Ram,
Katiyar Santosh K.,
Yusuf Nabiha,
Elmets Craig A.,
Xu Hui
Publication year - 2014
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/php.12351
Subject(s) - immunosuppression , immune system , immunology , chemokine , immune tolerance , myeloid , population , cancer research , immunotherapy , biology , medicine , environmental health
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 CD 11b 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.