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Stevens-Johnson综合征/中毒性表皮坏死松解症角质形成细胞死亡机制的研究进展 被引量：1

Mechanisms of keratinocyte death in Stevens-Johnson syndrome/toxic epidermal necrolysis
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摘要 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. 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.
作者 杨永生 徐金华
机构地区 复旦大学附属华山医院皮肤科
出处 《国际皮肤性病学杂志》 2015年第1期48-50,共3页 International Journal of Dermatology and Venereology
关键词 STEVENS-JOHNSON综合征 表皮坏死松解症 中毒性 角蛋白细胞 细胞凋亡 Stevens-Johnson syndrome Epidermal necrolysis,toxic Keratinocytes Apoptosis
分类号 R758.2 [医药卫生—皮肤病学与性病学]
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参考文献16

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同被引文献29

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国际皮肤性病学杂志
2015年 第1期

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