國家衛生研究院 NHRI:Item 3990099045/15583
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    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/15583


    Title: Inhibition of SARS-CoV-2-mediated thromboinflammation by CLEC2.Fc
    Authors: Hsieh, SL
    Contributors: Immunology Research Center
    Abstract: Thromboinflammation is the major cause of morbidity and mortality in COVID-19 patients, and post-mortem examination demonstrates the presence of platelet-rich thrombi and microangiopathy in lung and other visceral organs. Moreover, persistent microclots were detected in both acute COVID-19 and long COVID plasma samples. However, the molecular mechanism of SARS-CoV-2-induced thromboinflammation is still unclear. We found that the spleen tyrosine kinase (Syk)-coupled C-type lectin member 2 (CLEC2), which was highly expressed in platelets, interacted with the receptor-binding domain (RBD) of SARS-CoV-2 spike protein (SARS-CoV-2 RBD) directly. Unlike the thread-like NETs, SARS-CoV-2-induced aggregated NET formation in the presence of wild-type (WT), but not CLEC2-deficient platelets. Furthermore, SARS-CoV-2 spike pseudotyped lentivirus was able to induce NET formation via CLEC2, indicating SARS-CoV-2 RBD engaged CLEC2 to activate platelets to enhance NET formation. Administration of CLEC2.Fc inhibited SARS-CoV-2-induced NET formation and thromboinflammation in AAV-ACE2-infected mice. Thus, CLEC2 is a novel pattern recognition receptor for SARS-CoV-2, and CLEC2.Fc is a promising therapeutic agent to inhibit SARS-CoV-2-induced thromboinflammation and reduced the risk of post-acute sequelae of COVID (PASC) in the future.
    Date: 2023-05-01
    Relation: Journal of Immunology. 2023 May 01;210(Suppl. 1):Abstract number 236.02.
    Link to: http://dx.doi.org/10.4049/jimmunol.210.Supp.236.02
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0022-1767&DestApp=IC2JCR
    Appears in Collections:[Shie-Liang Hsieh] Conference Papers/Meeting Abstract

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