Premium
Differential Roles of T‐cell Subsets in Regulation of Ultraviolet Radiation Induced Cutaneous Photocarcinogenesis
Author(s) -
Nasti Tahseen H.,
Iqbal Omer,
Tamimi Iman A.,
Geise James T.,
Katiyar Santosh K.,
Yusuf Nabiha
Publication year - 2010
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/j.1751-1097.2010.00859.x
Subject(s) - cd8 , skin cancer , carcinogenesis , immunosuppression , cancer research , biology , immunology , t cell , microbiology and biotechnology , cancer , immune system , genetics
Abstract Ultraviolet (UV) radiation, in particular the midwavelength range (UVB; 290–320 nm), is one of the most significant risk factors for the development of nonmelanoma skin cancer. UVB radiation‐induced immunosuppression, which occurs in both humans and laboratory animals, contributes to their pathogenesis. However, there are conflicting reports on the relative role of CD4 + and CD8 + T cells in UVB induced skin cancer. The purpose of this study was to delineate the contribution of these two cell subpopulations to UVB induced immunosuppression and tumor development using C3H/HeN (WT), CD4 knockout (CD4 −/− ) and CD8 knockout (CD8 −/− ) mice. We observed that UVB induced skin carcinogenesis was retarded in terms of number of tumors per group, tumor volume and percentage of mice with tumors, in mice deficient in CD4 + T cells compared with wild‐type mice, whereas significantly greater ( P < 0.05) numbers of tumors occurred in CD8 −/− mice. These results indicate that, CD4 + T cells promote tumor development while CD8 + T cells have the opposite effect. Further, we found that CD4 + T cells from tumor‐bearing mice produced interleukin (IL)‐4, IL‐10, and IL‐17 whereas CD8 + T cells produced interferon‐γ. Manipulation of T‐cell subpopulations that are induced by UVB radiation could be a means of preventing skin cancers caused by this agent.