Clinical and Translational Immunology: How do our skin heal after UV sunburn?

Introduction: Although the spring sun is not very hot, but the exquisite women under the mask is already a full set of makeup plus a thick layer of sunscreenTo be sure, multiple sun protection is necessaryUltraviolet rays in sunlight can have many adverse effects on the human body, such as induced inflammation, skin disease, and in severe cases even lead to skin immunosuppression and skin cancerSun-loving Americans spend billions of dollars a year on medical advice and treatment for skin cancerTherefore, interpreting how UV mediates the skin's immune microenvironment may suggest new ways of sun protection and repairThe Lesley Rhodes team at the University of Manchester in the United Kingdom recently published an important work in the journal Clinical translation al Immunology, which found that after the human skin was sunburned with ultraviolet rays, two T-cells, CD4 plus GATA3 and CD8 plus GATA3, were recruited to the surface of the skin and repaired for more than 14 days, suggesting that targeting these immune cells could prevent and accelerate the improvement of sunburn skin conditionsUltraviolet (UVR) radiation is exposed for long periods of time (about 4-6 hours), and our skin experiences red spots, pain and edema, which is the skin's self-decomposing inflammatory response to UV damageAfter inflammation, the tissue does not immediately return to steady state, but instead "adaptive steady state" occurs, at which point, immune cells will remain in the immune suppression environment to maintain the immunosuppressive environment, although the initial inflammatory signals have subsided, and the secondary immersion or inflammation subsidesPrevious studies have shown that regulatory T-cells (Tregs) are essential for skin immunosuppression after exposure to UVR in mice, but it is not known how human skin heals itselfso the researchers recruited a group of healthy volunteers to conduct experiments in the photobiology department at Salford Royal, University of Manchester, to safely expose a portion of the volunteers' skin to a single dose of uVR that causes inflammation;the human skin in the UVR exposure 4 days after cell decompositionresults show that the typical cell decomposition occurs 4 days after UVR exposure;here, researchers found in human skin that CD8-GATA3-T cells, unlike CD4-Tregs found in mouse models, were retained after inflammation, and the researchers speculated that they could increase the IL-10 content by promoting GATA3 expression, which increased the level of IL-10 to produce immunosuppressive activityIn other words, UVR-induced human inflammation also involves the "post-decomposition phase", when immune regulation remains at a high level, which means that the immune system is self-stabilized and repaired after UVR exposureexposure within 14 days, UVR-induced inflammation recruited and retained CD8-GATA3-T cellsfinally, the researchers still detected high immune activity in human skin 14 days after UVR exposure, indicating that prolonged immunosuppression after inflammatory stimulation helped prevent "adaptive stability" Specifically, after acute inflammation, the synthesis of prostaglandins and hydroxy acids increases, while CD8-GATA3-T cells are retained in the skin because uVR exposure releases a large number of potential autoantigens, these immune cells and mesosomes may be necessary to maintain an immunosuppressive environment and prevent chronic inflammation or autoimmune The researchers believe that increasing the activity of these immune cells (e.g CD4 plus / CD8 plus GATA3 cells) to increase the synthesis of IL-10 or M2M-sands, as well as manipulating lipid media, can accelerate the subsidence of inflammation and improve the skin microenvironment after UVR exposure leads to cell decomposition Within 14 days of UVR exposure, the synthesis of prostaglandins and hydroxy lacids increased Hawkshaw et al the results revealed an interesting phenomenon, namely, that immune cells of certain types (CD4 plus / CD8 plus GATA3) will remain on the skin surface for a period of time and participate in the skin self The defense and repair process, which will be an important target for the repair of sunburn and skin cancer prevention, and the results break through previous findings in mouse models, suggest that the mouse skin's response to UVR cannot be reasonably extrapolated into human skin, suggesting that skin care products and drugs for UVR need to be tested by humans to test their efficacy