Ultraviolet Induced Skin Inflammation

Abstract

Abstract. Ultraviolet (UV) induced skin inflammation (UISI) is associated with many skin disorders. However, the mechanism by which UV causes skin inflammation remains unclear. Studies evaluating UISI in vivo have mainly been conducted using mouse models. Current investigations indicate that the classic inflammatory pathways involving nuclear factor kappa B and Toll-like receptor contribute to the regulation of UISI. However, more novel signaling factors have been identified as being involved in this process, including interleukin 22 receptor-α, cluster of differentiation 28 and cluster of differentiation 1d, serum amyloid A1, estrogen, melatonin, peroxisome proliferator activated receptors β/δ, isocitrate dehydrogenase 2, and transglutaminase 2. In addition, the gene mutation of fermitin family member 1 and selenium deficiency are reported to affect the phenotype of UISI. Although the actual roles of UISI in UV-related skin diseases need to be clarified, recent studies have reported the potent contribution of UISI to photocarcinogesis. To clarify the process and modulation of UISI, the special profiles of cytokines and inflammatory mediators and the core regulatory pathways should be identified clearly. These investigations would be promoted rapidly, accompanied by the conduction of high-quality clinical research on patients with UV-related skin disease and the construction of precise animal models of UISI.