Recent evidence indicates that classic inflammatory pathways involving nuclear factor kappa B and Toll-like receptor contribute modulateultraviolet (UV)-induced skin inflammation (UISI). Yet, other signaling factors have been found to be involved in this process, for instance – 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. Furthermore, the gene mutation of fermitin family member 1 and selenium deficiency could impact the phenotype of UISI.

Recent studies report the potent contribution of UISI to photocarcinogenesis. The mechanism of UISI can be comprehended through the identification of special profiles of cytokines and inflammatory mediators and the core regulatory pathways. 

Future investigations should aim towards the clarifying the actual roles of UISI in UV-related skin diseases. High-quality clinical research is warranted on patients with such dermatological conditions.

Source: Int JDermatol Venereol. 2021;4(4):229-35.