CAJ | 학술논문

角质形成细胞的凋亡涉及代谢及免疫机制,前者可能是亲电子的药物活性代谢产物经线粒体途径诱导凋亡.Stevens-Johnson综合征免疫机制则较复杂,CD8+细胞毒T细胞、自然杀伤细胞、单核细胞及调节T细胞等免疫细胞参与发病.肿瘤坏死因子α、可溶性FasL、颗粒溶素、肿瘤坏死因子相关凋亡诱导配体和肿瘤坏死因子样弱凋亡因子等细胞因子参与了凋亡作用的放大.在角质形成细胞的坏死中,警报素家族成员S100A、α防御素、高迁移率族蛋白B1均参与.
각질형성세포적조망섭급대사급면역궤제,전자가능시친전자적약물활성대사산물경선립체도경유도조망.Stevens-Johnson종합정면역궤제칙교복잡,CD8+세포독T세포、자연살상세포、단핵세포급조절T세포등면역세포삼여발병.종류배사인자α、가용성FasL、과립용소、종류배사인자상관조망유도배체화종류배사인자양약조망인자등세포인자삼여료조망작용적방대.재각질형성세포적배사중,경보소가족성원S100A、α방어소、고천이솔족단백B1균삼여.
The apoptosis of keratinocytes involves drug metabolism and immune mechanism.The former mainly refers to the induction of apoptosis by active electrophilic drug metabolites through the mitochondrial pathway.Comparatively,the immune mechanism is more complex with the involvement of many immune cells including CD8+ cytotoxic T cells,natural killer cells,monocytes and regulatory T cells.Some cytokines,such as tumor necrosis factor α (TNF-o),soluble FasL,granulysin,TNF-related apoptosis-inducing ligand (TRAIL) and TNF-like weak inducer of apoptosis (TWEAK),contribute to the amplification of apoptosis.The necrosis of keratinocytes is considered to be associated with the alarm family members S100A,β-defensins and high mobility group protein B1.