马拉塞西亚环球菌通过诱导皮细胞的IL-23分泌来诱导致病性Th17细胞的分化
Qiuyu Jia1, Jian Hu1, Xiaojie Wang1
1Department of Dermatology, Peking University People's Hospital, No.11 Xizhimen South Street, Xicheng District, Beijing, 100044, China.
Mycopathologia
|September 16, 2024
概括
马拉塞西亚环球菌通过激活INTERLEUKIN-17 (IL-17) 途径,触发皮肤炎症. 这种真菌促进致病性T助手17 (Th17) 细胞分化,加剧炎症性皮肤疾病.
科学领域:
- 皮肤病学 皮肤病学
- 免疫学 免疫学 免疫学
- 微生物学 微生物学
背景情况:
- 马拉塞西亚是一种常见的皮肤真菌,与炎症性皮肤疾病有关.
- 了解马拉塞西亚在皮肤炎症中的作用对于开发向疗法至关重要.
研究的目的:
- 调查马拉塞西亚环球菌诱导皮肤炎症的机制.
- 阐明介素-17 (IL-17) 信号传递和T辅助细胞17 (Th17) 在马拉塞西亚诱导的炎症中的作用.
主要方法:
- 在小鼠皮肤上用Mlassezia globosa在皮肤上进行皮肤上应用.
- 用RNA测序小鼠皮肤病变来分析基因表达.
- 在体外实验中使用人类初级角质细胞和马拉塞西亚全球菌进行实验.
主要成果:
- 在小鼠中,Malassezia globosa的应用引发了皮肤炎症.
- RNA测序揭示了IL-17信号传递和Th17细胞分化途径的激活.
- 观察到IL-23,IL-23R,IL-17A和IL-22的上调,病原性Th17细胞的增加.
- 马拉塞西亚环球菌刺激质细胞通过TLR2/MyD88/NF-κB信号传导分泌IL-23,从而驱动致病性Th17细胞的分化.
结论:
- 马拉塞西亚环球菌在加剧皮肤炎症方面发挥着重要作用.
- 这项研究突出了涉及马拉塞西亚诱导的IL-23分泌由角质细胞和随后的致病性Th17细胞分化的途径.
- 这些发现提供了有关马拉塞西亚相关炎症性皮肤疾病的病原体的见解.
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