{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T10:51:41Z","timestamp":1790506301024,"version":"4.1.0"},"reference-count":65,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2020,12,8]],"date-time":"2020-12-08T00:00:00Z","timestamp":1607385600000},"content-version":"vor","delay-in-days":342,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100003323","name":"Agence Nationale de Recherches sur le Sida et les H\u00e9patites Virales","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100003323","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100008656","name":"Fondation Innovations en Infectiologie","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100008656","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Clin &amp; Trans Imm"],"published-print":{"date-parts":[[2020,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objectives<\/jats:title><jats:p>C\u2010type lectin receptors (CLRs) are key receptors used by DCs to orchestrate responses to pathogens. During infections, the glycan\u2013lectin interactions shape the virus\u2013host interplay and viruses can subvert the function of CLRs to escape antiviral immunity. Recognition of virus\/viral components and uptake by CLRs together with subsequent signalling cascades are crucial in initiating and shaping antiviral immunity, and decisive in the outcome of infection. Yet, the interaction of hepatitis B virus (HBV) with CLRs remains largely unknown. As HBV hijacks DC subsets and viral antigens harbour glycan motifs, we hypothesised that HBV may subvert DCs through CLR binding.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We investigated here the pattern of CLR expression on BDCA1<jats:sup>+<\/jats:sup> cDC2s, BDCA2<jats:sup>+<\/jats:sup> pDCs and BDCA3<jats:sup>+<\/jats:sup> cDC1s from both blood and liver of HBV\u2010infected patients and explored the ability of HBsAg to bind DC subsets through specific CLRs.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>We highlighted for the first time that the CLR repertoire of circulating and intrahepatic cDC2s, cDC1s and pDCs was perturbed in patients with chronic HBV infection and that some CLR expression levels correlated with plasma HBsAg and HBV DNA levels. We also identified candidate CLR responsible for HBsAg binding to cDCs (CD367\/DCIR\/CLEC4A, CD32\/Fc\u0263RIIA) and pDCs (CD369\/DECTIN1\/CLEC7A, CD336\/NKp44) and demonstrated that HBsAg inhibited DC functions in a CLR\u2010 and glycosylation\u2010dependent manner.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>HBV may exploit CLR pathways to hijack DC subsets and escape from immune control. Such advances bring insights into the mechanisms by which HBV subverts immunity and pave the way for developing innovative therapeutic strategies to restore an efficient immune control of the infection by manipulating the viral glycan\u2013lectin axis.<\/jats:p><\/jats:sec>","DOI":"10.1002\/cti2.1208","type":"journal-article","created":{"date-parts":[[2020,12,10]],"date-time":"2020-12-10T03:22:40Z","timestamp":1607570560000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Hepatitis B virus exploits C\u2010type lectin receptors to hijack cDC1s, cDC2s and pDCs"],"prefix":"10.1002","volume":"9","author":[{"given":"Laurissa","family":"Ouaguia","sequence":"first","affiliation":[{"name":"Institute for Advanced Biosciences, Immunobiology and Immunotherapy in Chronic Diseases Inserm U 1209 CNRS UMR 5309 Universit\u00e9 Grenoble Alpes Grenoble France"},{"name":"R&amp;D Laboratory Etablissement Fran\u00e7ais du Sang 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