药疹是一种常见的迟发型超敏反应,通常有3种理论解释其发生机制,即药物半抗原、前半抗原和p-i理论,而药物特异性的细胞毒性T淋巴细胞在其病理过程中至关重要。经典理论认为,细胞毒性T淋巴细胞主要为CD8+T细胞,但是有证据表明,CD4+T细胞等其他表型的免疫细胞也具有细胞毒性,在药疹发病过程中发生特异性激活,接触靶细胞并释放毒性分子。靶细胞能够为药物代谢、炎症发生和自身凋亡提供有利环境,协助细胞毒性T淋巴细胞发挥作用。另外,“危险信号假说”认为危险信号在免疫激活中具有重要的作用,进一步补充完善药疹的发病机制。
Drug eruption is a common delayed hypersensitivity reaction. Its pathogenesis can be usually explained by three theories, including haptens, pro-haptens and pharmacological interaction with immune receptors (the p-i concept). Drug-specific eytotoxic T lymphocytes (CTLs) play an important role in the pathological process of drug eruption. In classic theories, CTLs are commonly recognized as CD8^+ T cells, but new evidences indicate that other immune cells with different phenotypes, such as CD4^+ T cells, also have cytotoxicity. In the development of drug eruption, these immune cells are specifically activated to contact with target cells followed by the release of cytotoxins. Target cells can provide a favoring environment for the metabolism of drugs and occurrence of inflammation and apoptosis, and assist CTLs to function. In addition, the danger signal hypothesis suggests that danger signals play an important role in immune activation, which enriches our knowledge on the pathogenesis of drug eruption.