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抗病毒CD8+ T细胞免疫反应受到香烟烟雾和COPD的损害
Jie Chen1,2,3,4, Xinyuan Wang1,5,4, Adrian Schmalen6,7
1Institute of Lung Health and Immunity and Comprehensive Pneumology Center with the CPC-M bioArchive, Helmholtz Zentrum München, Member of the German Center for Lung Research (DZL), Munich, Germany.
The European respiratory journal
|June 29, 2023
概括
香烟烟雾会损害免疫系统对抗病毒的能力,因为它会破坏T细胞识别受感染细胞的方式. 这导致吸烟者和COPD患者的T细胞数量减少,增加感染易感性.
科学领域:
- 免疫学 免疫学 免疫学
- 呼吸系统医学 呼吸系统医学
- 分子生物学分子生物学
背景情况:
- 病毒感染加剧了慢性阻塞性肺病 (COPD).
- 抗病毒免疫依赖于CD8+T细胞识别由MHCI类分子呈现的病毒表位.
- 免疫蛋白酶产生这些病毒表位,其诱导是由抗病毒细胞因子驱动的.
研究的目的:
- 在病毒感染期间调查香烟烟雾对免疫蛋白酶和CD8+T细胞激活的影响.
- 了解香烟烟雾影响肺细胞抗原呈现的机制.
- 为了比较COPD患者的T细胞反应与健康个人和喘患者.
主要方法:
- 通过细胞因子和流感A病毒 (IAV) 诱导肺细胞暴露于香烟烟雾中的免疫蛋白酶的分析 (体外,活体外,活体内).
- 使用与IAV感染细胞的共同培养试验评估CD8+T细胞激活.
- 质谱分析MHC I类结合和四聚体技术来量化患者的IAV特异性CD8+T细胞.
主要成果:
- 香烟烟雾显著损害了细胞因子和病毒感染的免疫蛋白酶诱导.
- 在暴露于烟雾的肺细胞中观察到MHC I类分子上呈现的改变谱.
- 香烟烟雾减少了IAV特异性CD8+T细胞的MHC I类中介激活.
- 与对照组相比,COPD患者的循环IAV特异性CD8+T细胞数量较少.
结论:
- 香烟烟雾干扰病毒抗原的生成和呈现通过MHC I类.
- 这种干扰导致CD8+T细胞激活受损,导致吸烟者和COPD患者对病毒感染的易感性增加.
- 这项研究提供了关于吸烟如何加剧呼吸道疾病中的病毒感染的机制性见解.
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