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CD3\n                    <jats:sup>+<\/jats:sup>\n                    CD56\n                    <jats:sup>+<\/jats:sup>\n                    NKT\u2010like cells play an important role in antiviral immune response. However, the mechanism of NKT\u2010like cells to mediate immune tolerance remains largely elusive. In this study, we observed circulating NKT\u2010like cells from IC and IT CHB patients were phenotypically and functionally impaired, manifested by increased expression of inhibitory receptor TIGIT and decreased capacity of secreting antiviral cytokines. Besides, TIGIT\n                    <jats:sup>+<\/jats:sup>\n                    NKT\u2010like cells of IC and IT CHB patients expressed lower levels of cytotoxic cytokines than the TIGIT\n                    <jats:sup>\u2212<\/jats:sup>\n                    subset. Furthermore, increased expression of CD155, the ligand of TIGIT, on plasmacytoid dendritic cells (pDCs) was detected in IC and IT CHB patients. Importantly, the co\u2010culture of NKT\u2010like cells and pDCs showed that NKT\u2010like cells restored their antiviral ability after TIGIT blockade upon HBV peptide stimulation in IC and IT CHB patients. In conclusion, our findings suggest that the TIGIT pathway may mediate immune tolerance in IT CHB patients and lead to functional impairment in IC patients, indicating that TIGIT may be a potential therapeutic checkpoint for immunotherapy of CHB patients.\n                  <\/jats:p>","DOI":"10.1002\/eji.202451046","type":"journal-article","created":{"date-parts":[[2024,5,23]],"date-time":"2024-05-23T01:15:56Z","timestamp":1716426956000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Restoration of CD3\n                    <sup>+<\/sup>\n                    CD56\n                    <sup>+<\/sup>\n                    NKT\u2010like cell function by TIGIT blockade in inactive carrier and immune tolerant patients of chronic hepatitis B virus infection"],"prefix":"10.1002","volume":"54","author":[{"given":"Xiaojing","family":"Yu","sequence":"first","affiliation":[{"name":"Department of Clinical Laboratory The First Affiliated Hospital of Anhui Medical University  Hefei China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuanling","family":"Zheng","sequence":"additional","affiliation":[{"name":"Department of Clinical Laboratory The First Affiliated Hospital of Anhui Medical University  Hefei China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ruoyu","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Clinical Laboratory The First Affiliated Hospital of Anhui Medical University  Hefei China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoran","family":"Dai","sequence":"additional","affiliation":[{"name":"Department of Clinical Laboratory The First Affiliated Hospital of Anhui Medical University  Hefei China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guijie","family":"Kang","sequence":"additional","affiliation":[{"name":"Inflammation and Immune\u2010Mediated Diseases Laboratory of Anhui 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