痤疮丙酸杆菌通过辅助性T淋巴细胞17炎症通路致寻常痤疮的机制研究进展
Research progress on mechanisms of Cutibacterium acnes inducing acne vulgaris via Th17 inflammatory pathway
王羽侬 1孙娅楠 2任星 2周娜 2王毅2
作者信息
- 1. 100029 北京,北京中医药大学第三附属医院皮肤科
- 2. 中国中医科学院医学实验中心
- 折叠
摘要
寻常痤疮是一种常见的慢性炎症性皮肤病,皮脂分泌旺盛、毛囊角化过度、皮肤菌群失调和局部免疫炎症反应是寻常痤疮发生的重要因素.近年来对痤疮发生机制的研究成果包括:痤疮丙酸杆菌(C acnes)生物膜形成与体内毒力因子增强有关;C acnes多样性下降,令IA1型C.acnes占主导地位,从而诱导辅助性T淋巴细胞17(Th17)通路激活,角质形成细胞、成纤维细胞、单核细胞和皮脂细胞在痤疮炎症反应中发挥核心作用.该文就C acnes诱发Th17炎症通路激活导致痤疮的发病机制进行综述.
Abstract
Acne vulgaris is a common chronic inflammatory skin disease.The important pathogenic factors of acne vulgaris include high sebum secretion,hyperkeratosis of hair follicles,dysregulation of skin flora and local immune inflammatory reaction.Recent studies on the mechanisms underlying acne occurrence have shown that the biofilm formation of Cutibacterium acnes(C.acnes)is related to increased in vivo virulence factors;The decline in C.acnes diversity led to the dominance of type IA1 C.acnes,subsequently inducing the activation of helper T cells 17(Th17)pathway.In addition,keratinocytes,fibroblasts,monocytes and sebum cells play pivotal roles in the inflammatory response of acne.In this paper,the pathogenesis of acne,triggered by the activation of Th 17 inflammatory pathway induced by C.acnes,was comprehensively reviewed.
关键词
痤疮/痤疮丙酸杆菌/Th17细胞/炎症/发病机制Key words
Acne/Cutibacterium acnes/Th17 cells/Inflammation/Pathogenesis引用本文复制引用
出版年
2024
NETL
NSTL
万方数据