Pathophysiological Mechanisms of UVB Irradiation in the Skin: Inflammation, Oxidative Stress and Neuroimmune Interactions

Ultraviolet B (UVB) irradiation, with wavelengths ranging from 290 to 320 nm, represents a biologically active fraction of solar irradiation that reaches the Earth’s surface and exerts significant effects on human skin. Due to its high energy, UVB penetrates the epidermis and directly interacts with cellular components, particularly DNA, leading to the formation of photoproducts such as cyclobutane pyrimidine dimers. In parallel, UVB exposure induces the generation of reactive oxygen species, promoting oxidative stress and damage to lipids, proteins, and genetic material. These events activate key intracellular signaling pathways, including NF-κB and MAPKs, resulting in the production of pro-inflammatory mediators that amplify cutaneous inflammation. In addition to classical inflammatory and oxidative mechanisms, emerging evidence highlights the role of neuroimmune interactions in the skin, involving crosstalk between nerve endings, neuropeptides, and immune cells, which contributes to the regulation of local immune responses following UVB exposure. The integration of these processes plays a central role in the pathophysiology of UVB-induced skin damage and in the development of skin diseases. This review will discuss the molecular and cellular mechanisms underlying the cutaneous response triggered by UVB irradiation, with emphasis on inflammation, oxidative stress, and neuroimmune communication. Additionally, current and emerging therapeutic strategies based on pathophysiology mechanisms, including antioxidant agents, anti-inflammatory compounds, and photoprotective approaches, will be discussed to highlight potential avenues for improved prevention and treatment of UVB-induced skin damage.