Zhang Jia-Xiang, Li Na, Wang Hui, Shen Tong, Zhu Qi-Xing
1 Institute of Dermatology, Anhui Medical University, Anhui, China.
2 Department of Occupational Health and Environment Health, School of Public Health, Anhui Medical University, Anhui, China.
Toxicol Ind Health. 2017 Nov;33(11):876-883. doi: 10.1177/0748233717731213. Epub 2017 Oct 11.
Trichloroethylene (TCE) has been used for a variety of industrial and consumer cleaning purposes because of its ability to dissolve organic substances. The multisystem injuries include those of skin, liver, and kidney, which are defined as TCE hypersensitivity syndrome (THS). THS is a serious occupational health issue. However, the mechanism of immune dysfunction leading to organ injury is poorly understood. Many studies reveal that skin lesions and organ injury caused by TCE are consistent with type IV hypersensitivity, also called delayed hypersensitivity, mediated by T cells. However, many researchers found T cell-mediated type IV hypersensitivity could not account for the pathogenesis of THS fully. Humoral immunity, including immunoglobulins and complement activation, may also play a possible role in THS pathogenesis. This review will describe the history, current understanding, and future research directions of the mechanism of THS.
三氯乙烯（TCE）因其具有溶解有机物质的能力，已被用于各种工业和消费清洁用途。多系统损伤包括皮肤、肝脏和肾脏损伤，这些被定义为三氯乙烯超敏综合征（THS）。THS是一个严重的职业健康问题。然而，导致器官损伤的免疫功能障碍机制尚不清楚。许多研究表明，TCE引起的皮肤病变和器官损伤与IV型超敏反应一致，也称为迟发型超敏反应，由T细胞介导。然而，许多研究人员发现，T细胞介导的IV型超敏反应不能完全解释THS的发病机制。体液免疫，包括免疫球蛋白和补体激活，也可能在THS发病机制中发挥作用。本综述将描述THS机制的历史、当前认识和未来研究方向。
