Abstract
Skin cancer is the most common cancer in the USA with ultraviolet radiation (UVR) exposure being the major environmental risk factor. The mechanism by which UVR causes cancer is not yet clear but involves direct and indirect DNA damage, as well as local and systemic immunosuppression leading to a tumorigenic environment. At the cellular level, dermal dendritic cells, Langerhans cells, skin-infiltrating monocyte/macrophages, T lymphocytes, chemokines and cytokines participate. Dermal dendritic cells are recognized as the main antigen presenting cell of the skin. UV-induced skin-infiltrating monocytes/macrophages may be a source for these dermal dendritic cells. Langerhans cells serve an immunosuppressive role and activate regulatory T cells upon UVR damage. CD4+CD25+ regulatory T lymphocytes, upon activation by UV damage, suppress effector T lymphocyte proliferation, maturation and function, leading to decreased contact hypersensitivity responses. IL-12, a cytokine suppressed by UVR, is involved in DNA repair and is associated with decreased UV-induced immunosuppression, while IL-10, which is secreted in response to UVR, increases immunosuppression. This article will focus on current research into the mechanism of UV immunosuppression and its impact on skin cancers.
Financial & competing interests disclosure
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
No writing assistance was utilized in the production of this manuscript.