银屑病相关的 CCL27/CCR10 衍生调节受损导致产生 IL-17A/IL-22 的皮肤 T 细胞过度激活。
Psoriasis-associated impairment of CCL27/CCR10-derived regulation leads to IL-17A/IL-22-producing skin T-cell overactivation.
机构信息
Department of Microbiology, Immunology and Molecular Genetics, University of Texas Health Science Center San Antonio, San Antonio, Tex; Department of Veterinary and Biomedical Sciences, Centre for Molecular Immunology and Infectious Disease, The Pennsylvania State University, University Park, Pa; Division of Pneumoconiosis, School of Public Health, China Medical University, Shenyang, China.
Department of Veterinary and Biomedical Sciences, Centre for Molecular Immunology and Infectious Disease, The Pennsylvania State University, University Park, Pa.
出版信息
J Allergy Clin Immunol. 2021 Feb;147(2):759-763.e9. doi: 10.1016/j.jaci.2020.05.044. Epub 2020 Jun 10.
Abstract
Psoriasis-associated suppression of the skin-specific chemokine/receptor CCL27/CCR10 axis leads to enhanced pathogenic IL-17A/IL-22-producing skin T cell activation and inflammation.
摘要
银屑病相关的皮肤特异性趋化因子/受体 CCL27/CCR10 轴的抑制导致致病性的 IL-17A/IL-22 产生的皮肤 T 细胞激活和炎症增强。
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