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Moreover, persistent microclots were detected in both acute COVID\u201019 and long COVID plasma samples. However, the molecular mechanism of SARS\u2010CoV\u20102\u2010induced thromboinflammation is still unclear. We found that the spleen tyrosine kinase (Syk)\u2010coupled C\u2010type lectin member 2 (CLEC2), which was highly expressed in platelets and alveolar macrophages, interacted with the receptor\u2010binding domain (RBD) of SARS\u2010CoV\u20102 spike protein (SARS\u2010CoV\u20102 RBD) directly. Unlike the thread\u2010like NETs, SARS\u2010CoV\u20102\u2010induced aggregated NET formation in the presence of wild\u2010type (WT), but not CLEC2\u2010deficient platelets. Furthermore, SARS\u2010CoV\u20102 spike pseudotyped lentivirus was able to induce NET formation via CLEC2, indicating SARS\u2010CoV\u20102 RBD engaged CLEC2 to activate platelets to enhance NET formation. Administration of CLEC2.Fc inhibited SARS\u2010CoV\u20102\u2010induced NET formation and thromboinflammation in AAV\u2010ACE2\u2010infected mice. Thus, CLEC2 is a novel pattern recognition receptor for SARS\u2010CoV\u20102, and CLEC2.Fc and may become a promising therapeutic agent to inhibit SARS\u2010CoV\u20102\u2010induced thromboinflammation and reduced the risk of post\u2010acute sequelae of COVID\u201019 (PASC) in the future.<\/jats:p>","DOI":"10.15252\/emmm.202216351","type":"journal-article","created":{"date-parts":[[2023,5,22]],"date-time":"2023-05-22T03:50:22Z","timestamp":1684727422000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Inhibition of SARS\u2010CoV\u20102\u2010mediated thromboinflammation by CLEC2.Fc"],"prefix":"10.1038","volume":"15","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5061-4989","authenticated-orcid":false,"given":"Pei\u2010Shan","family":"Sung","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Cheng\u2010Pu","family":"Sun","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mi\u2010Hua","family":"Tao","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9415-346X","authenticated-orcid":false,"given":"Shie\u2010Liang","family":"Hsieh","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2023,5,22]]},"reference":[{"key":"BFEMMM202216351_CR1","doi-asserted-by":"crossref","first-page":"1156","DOI":"10.1021\/acscentsci.0c01537","volume":"7","author":"R Amraei","year":"2021","unstructured":"Amraei R, Yin W, Napoleon MA, Suder EL, Berrigan J, Zhao Q, Olejnik J, Chandler KB, Xia C, Feldman J et\u00a0al (2021) CD209L\/L\u2010SIGN and CD209\/DC\u2010SIGN act as receptors for SARS\u2010CoV\u20102. 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