title: Interleukin-17 mediated inflammatory responses are required for ultraviolet radiation-induced immune suppression.
abstract: 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.
authors.affiliation: Department of Dermatology, University of Alabama at Birmingham, Birmingham, AL.
authors.forename: Hui
authors.initials: H
authors.lastname: Li
authors.forename: Ram
authors.initials: R
authors.lastname: Prasad
authors.forename: Santosh K
authors.initials: SK
authors.lastname: Katiyar
authors.forename: Nabiha
authors.initials: N
authors.lastname: Yusuf
authors.forename: Craig A
authors.initials: CA
authors.lastname: Elmets
authors.forename: Hui
authors.initials: H
authors.lastname: Xu
mesh_terms: D000818:Animals; D007165:Immunosuppression Therapy; D007249:Inflammation / Q000503:physiopathology*; D020381:Interleukin-17 / Q000502:physiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D053722:Receptors, Interleukin-17 / Q000235:genetics / Q000502:physiology; D014466:Ultraviolet Rays
chemical_list: D020381:Interleukin-17; D053722:Receptors, Interleukin-17