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一种临床相关的STING激动剂抑制了人类T_H17细胞炎症特征

Luis Eduardo Alves Damasceno¹, Thiago Mattar Cunha², Fernando Queiroz Cunha²

¹Department of Pharmacology, Ribeirao Preto Medical School, University of Sao Paulo, Ribeirao Preto, SP 14049-900, Brazil; Center for Research in Inflammatory Diseases, Ribeirao Preto Medical School, University of Sao Paulo, Ribeirao Preto, SP 14049-900, Brazil; Institute of Medical Microbiology and Hygiene, University Medical Center of the Johannes Gutenberg-University, Mainz 55131, Germany.

International immunopharmacology

|October 1, 2023

概括

刺痛激动剂,如2'3'-c-di-AM(PS) 2(Rp,Rp),可以减少炎症T助手17 (T_H17) 细胞的反应. 这表明治疗由T_H17细胞介导的慢性炎症疾病的潜力.

科学领域:

免疫学免疫学免疫学
分子生物学分子生物学
炎症研究炎症研究

背景情况:

刺痛信号通路对于对病原体和瘤的免疫反应至关重要.
在小鼠模型中,STING激活在减弱自身免疫反应方面表现有希望,特别是那些涉及T辅助17 (T_H17) 细胞的细胞.
以前的研究表明,STING在体外限制了小鼠T_H17细胞的促炎程序.

研究的目的:

调查STING激动剂2'3'-c-di-AM (PS) 2 (Rp,Rp) 对分化人类T_H17细胞的影响.
确定STING激活能否调节T_H17细胞功能,并可能影响其他免疫细胞群.

主要方法:

用STING激动剂2'3'-c-di-AM (PS) 2 (Rp,Rp) 对分化的人类T_H17细胞的治疗.
在治疗的T_H17细胞中分析IL-17A的产生和IL23R的表达.
在STING激活下对调节性T (T_reg) 细胞生成的评估.

主要成果:

刺痛激动剂2'3'-c-di-AM (PS) 2 (Rp,Rp) 成功激活了在分化人类T_H17细胞中的刺痛信号体.
用2'3'-c-di-AM (PS) 2 (Rp,Rp) 的治疗导致人类T_H17细胞的IL-17A产生和IL23R表达显著减少.
STING激活促进了调节性T (T_{reg>) 细胞的产生.}

结论:

刺痛激动剂,以2'3'-c-di-AM (PS) 2 (Rp,Rp) 为例,可以通过减少促炎媒介来调节人类T_H17细胞的反应.
兴奋剂激动剂有利于T_reg细胞生成的能力表明一种潜在的治疗策略.
这些发现凸显了STING激动剂治疗人类T_H17介导慢性炎症疾病的治疗潜力.

关键词:

2′3′-c-di-AM ((PS) ((2) ((Rp,Rp)) 是一个字.在ADU-S100中使用.人类T(H) 17细胞时间时间时间刺痛是一种刺痛.

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