Lipid mediators of inflammation play important roles in several diseases including skin cancer, the most prevalent type of cancer found in the industrialized world. Ultraviolet (UV) radiation is a complete carcinogen and is the primary cause of skin cancer. UV radiation is also a potent immunosuppressive agent, and UV-induced immunosuppression is a well-known risk factor for skin cancer induction. An essential mediator in this process is the glyercophosphocholine 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine commonly referred to as platelet-activating factor (PAF). PAF is produced by keratinocytes in response to diverse stimuli and exerts its biological effects by binding to a single specific G-protein-coupled receptor (PAF-R) expressed on a variety of cells. This review will attempt to describe how this lipid mediator is involved in transmitting the immunosuppressive signal from the skin to the immune system, starting from its production by keratinocytes, to its role in activating mast cell migration in vivo, and to the mechanisms involved that ultimately lead to immune suppression. Recent findings related to its role in regulating DNA repair and activating epigenetic mechanisms, further pinpoint the importance of this bioactive lipid, which may serve as a critical molecular mediator that links the environment (UVB radiation) to the immune system and the epigenome.

炎症的脂质介体在多种疾病中起着重要作用，其中包括皮肤癌，这是工业化国家中发现的最普遍的癌症。紫外线（UV）是一种完全的致癌物质，是皮肤癌的主要原因。紫外线辐射也是一种有效的免疫抑制剂，紫外线诱导的免疫抑制是引起皮肤癌的众所周知的危险因素。在此过程中，必不可少的介质是甘油磷酸胆碱1-烷基-2-乙酰基-锡-甘油-3-磷酸胆碱通常称为血小板活化因子（PAF）。PAF由角质形成细胞响应各种刺激而产生，并通过与多种细胞上表达的单个特异性G蛋白偶联受体（PAF-R）结合而发挥其生物学作用。这篇综述将试图描述这种脂质介体如何参与从皮肤向免疫系统传递免疫抑制信号，从其由角质形成细胞产生开始，到其在体内激活肥大细胞迁移的作用，以及最终涉及的机制。导致免疫抑制。与它在调节DNA修复和激活表观遗传机制中的作用有关的最新发现进一步明确了这种生物活性脂质的重要性，