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辅助 T 细胞 17 免疫应答在冠状病毒免疫病理学和疫苗诱导免疫增强中的潜在作用。

The potential role of Th17 immune responses in coronavirus immunopathology and vaccine-induced immune enhancement.

机构信息

Texas Children's Hospital Center for Vaccine Development, Department of Pediatrics and Molecular Virology & Microbiology, National School of Tropical Medicine, Baylor College of Medicine, Houston, TX, USA; Department of Biology, Baylor University, Waco, TX, USA; Hagler Institute of Advanced Study at Texas A&M University, College Station, TX, USA.

Texas Children's Hospital Center for Vaccine Development, Department of Pediatrics and Molecular Virology & Microbiology, National School of Tropical Medicine, Baylor College of Medicine, Houston, TX, USA; Department of Biology, Baylor University, Waco, TX, USA.

出版信息

Microbes Infect. 2020 May-Jun;22(4-5):165-167. doi: 10.1016/j.micinf.2020.04.005. Epub 2020 Apr 17.

DOI:10.1016/j.micinf.2020.04.005
PMID:32305501
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7162764/
Abstract

Increasing evidence points to host Th17 inflammatory responses as contributing to the severe lung pathology and mortality of lower respiratory tract infections from coronaviruses. This includes host inflammatory and cytokine responses to COVID-19 caused by the SARS-2 coronavirus (SARS CoV2). From studies conducted in laboratory animals, there are additional concerns about immune enhancement and the role of potential host immunopathology resulting from experimental human COVID-19 vaccines. Here we summarize evidence suggesting there may be partial overlap between the underlying immunopathologic processes linked to both coronavirus infection and vaccination, and a role for Th17 in immune enhancement and eosinophilic pulmonary immunopathology. Such findings help explain the link between viral-vectored coronavirus vaccines and immune enhancement and its reduction through alum adjuvants. Additional research may also clarify links between COVID-19 pulmonary immunopathology and heart disease.

摘要

越来越多的证据表明,宿主 Th17 炎症反应可能导致冠状病毒引起的下呼吸道感染的严重肺部病理和死亡率升高。这包括宿主对 SARS-2 冠状病毒(SARS-CoV2)引起的 COVID-19 的炎症和细胞因子反应。从在实验动物中进行的研究中,人们对免疫增强以及潜在的宿主免疫病理学的作用产生了更多的担忧,这些作用来自于实验性的人类 COVID-19 疫苗。在这里,我们总结了一些证据,表明与冠状病毒感染和疫苗接种相关的潜在免疫病理过程之间可能存在部分重叠,并且 Th17 在免疫增强和嗜酸性粒细胞性肺免疫病理学中发挥作用。这些发现有助于解释病毒载体冠状病毒疫苗与免疫增强之间的联系,以及铝佐剂对此的降低作用。进一步的研究还可能阐明 COVID-19 肺部免疫病理学与心脏病之间的联系。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f023/7162764/fe5763e633e1/gr1_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f023/7162764/fe5763e633e1/gr1_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f023/7162764/fe5763e633e1/gr1_lrg.jpg

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