肿瘤坏死因子、Ⅰ型干扰素及白细胞介素23/17轴在银屑病的交互作用被引量：1

Interaction between tumor necrosis factor, type Ⅰ interferon and the interleukin-23/17 axis in psoriasis

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摘要银屑病是一种慢性复发性炎症性皮肤病，其发病的确切机制虽未完全阐明，但已有的证据表明与免疫相关。遗传学和免疫学研究表明，银屑病的发展和维持涉及多种细胞、多个分子和多条通路。因此，单一的靶向治疗似乎不能完全阻断其复杂的病理生理过程，而且可能引起患者免疫系统细胞因子间的不平衡。肿瘤坏死因子、Ⅰ型干扰素以及白细胞介素23/17轴是银屑病发病相关的重要因子，3种细胞因子在疾病过程中呈交互影响。 Psoriasis is a chronic recurrent inflammatory skin disease. Although the exact pathogenesis of psoriasis remains unclear, current evidence has indicated that it is associated with immunity. Both genetic and immunological researches demonstrate that the occurrence and maintenance of psoriasis involve a variety of cells, molecules and signaling pathways. Thus, single-targeted therapies seem not to be able to completely block the complex pathophysiologic processes of psoriasis, and may cause imbalance between cytokines in immune system of patients. Tumor necrosis factor （TNF）, type I interferon （IFN） and the interleukin （IL）-23/17 axis are important factors involved in the pathogenesis of psoriasis, and interact with each other in the development of psoriasis.

作者张加芬李新宇

机构地区中国医学科学院北京协和医学院皮肤病研究所药物研究室

出处《国际皮肤性病学杂志》 2016年第4期216-218,共3页 International Journal of Dermatology and Venereology

关键词银屑病肿瘤坏死因子类干扰素Ⅰ型白细胞介素23 白细胞介素17 交互分析 Psoriasis Tumor necrosis factors Interferon type Ⅰ Interleukin-23 Interleukin-17 Transactional analysis

分类号 R758.63 [医药卫生—皮肤病学与性病学]

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