在感染和自身免疫中表达CXCR3的T细胞
Artem Rubinstein1,2, Igor Kudryavtsev1,2, Natalia Arsentieva3
1Department of Immunology, Medical Faculty, First Saint Petersburg State I. Pavlov Medical University, 197022 Saint Petersburg, Russia.
Frontiers in bioscience (Landmark edition)
|August 29, 2024
概括
化基因受体CXCR3及其连接体是T细胞驱动炎症的关键,影响保护性免疫和自身免疫性疾病. 准CXCR3为各种疾病提供了潜在的治疗策略.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
- 分子医学是分子医学.
背景情况:
- CXCR3及其配体 (CXCL9,CXCL10,CXCL11) 是细胞炎症的核心.
- 在非免疫组织的淋巴细胞和细胞上表达CXCR3.
- 本综述侧重于表达CXCR3的T细胞子集.
研究的目的:
- 审查CXCR3表达T细胞在炎症中的作用.
- 突出外围组织中CXCR3依赖的相互作用.
- 探索CXCR3及其配体的治疗潜力.
主要方法:
- 对CXCR3和T细胞子集研究的文献综述.
- 对各种T细胞类型 (Th1,Th17.1,Tfh17,Tfh17.1,CXCR3+Treg,Tc1) 上CXCR3表达的分析.
- 检查CXCR3介导的免疫细胞的招募.
主要成果:
- 取决于CXCR3的相互作用协调了外围组织中的炎症.
- CXCR3促进炎症性CD4+和CD8+T细胞的招募.
- CXCR3促进调控T细胞的招募,以控制炎症.
结论:
- CXCR3及其配体是T细胞介导炎症的关键调节者.
- 了解这些途径可以导致新的治疗目标.
- 向CXCR3可能为炎症和自身免疫性疾病提供新的治疗方法.
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