Department of Dermatology, University Kiel, Schittenhelmstrasse 7, 24105 Kiel, Germany.
Eur J Cell Biol. 2011 Jun-Jul;90(6-7):560-4. doi: 10.1016/j.ejcb.2010.09.011. Epub 2010 Oct 29.
Solar ultraviolet radiation (UVR) is well known for its immunosuppressive properties. UVR can suppress immune reactions both in a local and a systemic fashion. One of the major molecular mediators of photoimmunosuppression is UVR-induced DNA damage. In contrast to immunosuppressive drugs, UVR does not act in a general but antigen-specific fashion. This is due to the induction of regulatory T cells. Epidermal Langerhans cells harboring UVR-induced DNA damage appear to be essentially involved in the induction of these cells. Cytokines including interleukin (IL)-12, -18 and -23 exert the capacity to reduce UVR-induced DNA damage via induction of DNA repair. Accordingly, these cytokines prevent UVR-mediated immunosuppression. In contrast to IL-18, IL-12 and IL-23 can also inhibit the suppressive activity of regulatory T cells by a mechanism which still needs to be determined. Clarification of the molecular mechanisms underlying UVR-induced immunosuppression will help to develop new immunosuppressive therapeutic strategies by utilizing UVR-induced regulatory T cells for the treatment of immune-mediated diseases. In addition, these insights will contribute to a better understanding of photocarcinogenesis since suppression of the immune system by UVR essentially contributes to the induction of skin cancer.
太阳紫外线辐射（UVR）以其免疫抑制特性而闻名。UVR 可以局部和全身方式抑制免疫反应。光致免疫抑制的主要分子介质之一是 UVR 诱导的 DNA 损伤。与免疫抑制药物不同，UVR 不是以普遍的方式，而是以抗原特异性的方式起作用。这是由于调节性 T 细胞的诱导。携带 UVR 诱导的 DNA 损伤的表皮朗格汉斯细胞似乎在诱导这些细胞中起主要作用。细胞因子，包括白细胞介素（IL）-12、-18 和 -23，通过诱导 DNA 修复来发挥减少 UVR 诱导的 DNA 损伤的能力。因此，这些细胞因子可以防止 UVR 介导的免疫抑制。与 IL-18 相反，IL-12 和 IL-23 还可以通过仍需确定的机制抑制调节性 T 细胞的抑制活性。阐明 UVR 诱导的免疫抑制的分子机制将有助于通过利用 UVR 诱导的调节性 T 细胞治疗免疫介导的疾病来开发新的免疫抑制治疗策略。此外，这些见解将有助于更好地理解光致癌作用，因为 UVR 对免疫系统的抑制实质上有助于皮肤癌的诱导。
