期刊论文详细信息
Frontiers in Microbiology
Toll-Like Receptor Signaling in Severe Acute Respiratory Syndrome Coronavirus 2-Induced Innate Immune Responses and the Potential Application Value of Toll-Like Receptor Immunomodulators in Patients With Coronavirus Disease 2019
Ziyuan Gao1  Jiayu Dai1  Yibo Wang1  Ying Wang1  Yingying Su2  Shuyou Shi3  Hua Wang3  Hongrui Wang3  Ming Yang3  Mingli Fang3  Peng Zhang4 
[1] College of Clinical Medicine, Jilin University, Changchun, China;Department of Anatomy, College of Basic Medical Sciences, Jilin University, Jilin, China;Department of Molecular Biology, College of Basic Medical Sciences, Jilin University, Changchun, China;Department of Thoracic Surgery, The First Affiliated Hospital of Jilin University, Changchun, China;
关键词: SARS-CoV-2;    COVID-19;    innate immune response;    Toll-like receptor;    immunomodulator;   
DOI  :  10.3389/fmicb.2022.948770
来源: DOAJ
【 摘 要 】

Toll-like receptors (TLRs) are key sensors that recognize the pathogen-associated molecular patterns (PAMPs) of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to activate innate immune response to clear the invading virus. However, dysregulated immune responses may elicit the overproduction of proinflammatory cytokines and chemokines, resulting in the enhancement of immune-mediated pathology. Therefore, a proper understanding of the interaction between SARS-CoV-2 and TLR-induced immune responses is very important for the development of effective preventive and therapeutic strategies. In this review, we discuss the recognition of SARS-CoV-2 components by TLRs and the downstream signaling pathways that are activated, as well as the dual role of TLRs in regulating antiviral effects and excessive inflammatory responses in patients with coronavirus disease 2019 (COVID-19). In addition, this article describes recent progress in the development of TLR immunomodulators including the agonists and antagonists, as vaccine adjuvants or agents used to treat hyperinflammatory responses during SARS-CoV-2 infection.

【 授权许可】

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