{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,31]],"date-time":"2026-03-31T03:00:15Z","timestamp":1774926015137,"version":"3.50.1"},"reference-count":50,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","license":[{"start":{"date-parts":[[2018,2,26]],"date-time":"2018-02-26T00:00:00Z","timestamp":1519603200000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Hepatology Communications"],"published-print":{"date-parts":[[2018,4]]},"abstract":"<jats:p>Autoimmune hepatitis (AIH) is an immune\u2010mediated liver disease currently treated by immunosuppressive medications with significant side effects. Thus, novel mechanistic treatments are greatly needed. We performed prospective deep immunophenotyping of blood immune cells in patients with acute AIH before and after corticosteroid therapy. Blood samples from 26 patients with acute AIH (United Kingdom\u2010AIH Consortium) were phenotyped by flow cytometry at baseline and 4 months after starting corticosteroids. Pretreatment liver tissues were stained for forkhead box P3\u2010positive (FOXP3<jats:sup>POS<\/jats:sup>) regulatory T cells (Tregs), clusters of differentiation (CD)56<jats:sup>POS<\/jats:sup> natural killer (NK) cells, and chemokine (C\u2010X\u2010C motif) ligand 10. Chemokine secretion by cultured primary hepatocyte and biliary epithelial cells was measured by enzyme\u2010linked immunosorbent assay. Functional coculture assays with stimulated NK cells and Tregs were performed. CD161 ligand, lectin\u2010like transcript\u20101 expression by intrahepatic immune cells was demonstrated with flow cytometry. Frequencies of NK<jats:sup>bright<\/jats:sup> cells declined with therapy (<jats:italic toggle=\"yes\">P<\/jats:italic> &lt; 0.001) and correlated with levels of alanine aminotransferase (<jats:italic toggle=\"yes\">P =<\/jats:italic> 0.023). The Treg:NK<jats:sup>bright<\/jats:sup> ratio was lower pretreatment, and Tregs had an activated memory phenotype with high levels of CD39, cytotoxic T lymphocyte antigen 4, and FOXP3 but also high programmed death ligand 1, indicating exhaustion. Coculture experiments suggested the Tregs could not efficiently suppress interferon\u2010\u03b3 secretion by NK cells. Both Tregs and NK cells had high expression of liver infiltration and T helper 17 plasticity\u2010associated marker CD161 (<jats:italic toggle=\"yes\">P =<\/jats:italic> 0.04). Pretreatment and CD161<jats:sup>pos<\/jats:sup> NK cells expressed high levels of perforin and granzyme B, consistent with an activated effector phenotype (<jats:italic toggle=\"yes\">P<\/jats:italic> &lt; 0.05). Lectin\u2010like transcript 1, a ligand for CD161, is expressed on intrahepatic B cells, monocytes, and neutrophils. <jats:italic toggle=\"yes\">Conclusion:<\/jats:italic> Activated effector NK cells, which correlate with biochemical measurements of hepatitis, and exhausted memory Tregs are increased in the blood of patients with treatment\u2010naive AIH and decline with corticosteroid therapy. Inadequate regulation of NK cells by exhausted FOXP3<jats:sup>pos<\/jats:sup> Tregs may play a role in AIH pathogenesis and contribute to liver injury. (<jats:italic toggle=\"yes\">Hepatology Communications<\/jats:italic> 2018;2:421\u2010436)<\/jats:p>","DOI":"10.1002\/hep4.1163","type":"journal-article","created":{"date-parts":[[2018,2,26]],"date-time":"2018-02-26T15:40:49Z","timestamp":1519659649000},"page":"421-436","source":"Crossref","is-referenced-by-count":39,"title":["Changes in natural killer cells and exhausted memory regulatory T Cells with corticosteroid therapy in acute autoimmune hepatitis"],"prefix":"10.1097","volume":"2","author":[{"given":"Hannah C.","family":"Jeffery","sequence":"first","affiliation":[{"name":"Centre for Liver Research, Institute of Immunology and Immunotherapy and National Institute of Health Research Inflammation Biomedical Research Centre Birmingham,University of Birmingham,Birmingham,United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Manjit K.","family":"Braitch","sequence":"additional","affiliation":[{"name":"Centre for Liver Research, Institute of Immunology and 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Birmingham,Birmingham,United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rebecca E.","family":"Wawman","sequence":"additional","affiliation":[{"name":"Centre for Liver Research, Institute of Immunology and Immunotherapy and National Institute of Health Research Inflammation Biomedical Research Centre Birmingham,University of Birmingham,Birmingham,United Kingdom"},{"name":"School of Life Sciences, Faculty of Health and Life Sciences,Coventry University,Coventry,United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lin Lee","family":"Wong","sequence":"additional","affiliation":[{"name":"Newcastle Biomedical Research Centre and Newcastle University,Newcastle,United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jane","family":"Birtwistle","sequence":"additional","affiliation":[{"name":"Clinical Immunology Department,University of Birmingham,Birmingham,United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Helen","family":"Bartlett","sequence":"additional","affiliation":[{"name":"Centre for Liver Research, Institute of Immunology and Immunotherapy and National Institute of Health Research Inflammation Biomedical Research Centre Birmingham,University of Birmingham,Birmingham,United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ansgar W.","family":"Lohse","sequence":"additional","affiliation":[{"name":"University of Hamburg,Hamburg,Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gideon M.","family":"Hirschfield","sequence":"additional","affiliation":[{"name":"Centre for Liver Research, Institute of Immunology and Immunotherapy and National Institute of Health Research Inflammation Biomedical Research Centre Birmingham,University of Birmingham,Birmingham,United Kingdom"},{"name":"Liver Transplantation and Hepatobiliary Unit, Queen Elizabeth Hospital,University Hospitals Birmingham National Health Service Foundation Trust,Birmingham,United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jessica","family":"Dyson","sequence":"additional","affiliation":[{"name":"Newcastle Biomedical Research Centre and Newcastle University,Newcastle,United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David","family":"Jones","sequence":"additional","affiliation":[{"name":"Newcastle Biomedical Research Centre and Newcastle University,Newcastle,United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Stefan G.","family":"Hubscher","sequence":"additional","affiliation":[{"name":"Centre for Liver Research, Institute of Immunology and Immunotherapy and National Institute of Health Research Inflammation Biomedical Research Centre Birmingham,University of Birmingham,Birmingham,United Kingdom"},{"name":"Department of Histopathology, Queen Elizabeth Hospital,University Hospitals Birmingham National Health Service Foundation Trust,Birmingham,United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Paul","family":"Klenerman","sequence":"additional","affiliation":[{"name":"Peter Medawar Building of Pathogen Research,University of Oxford,Oxford,United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6776-0336","authenticated-orcid":false,"given":"David H.","family":"Adams","sequence":"additional","affiliation":[{"name":"Centre for Liver Research, Institute of Immunology and Immunotherapy and National Institute of Health Research Inflammation Biomedical Research Centre Birmingham,University of Birmingham,Birmingham,United Kingdom"},{"name":"Liver Transplantation and Hepatobiliary Unit, Queen Elizabeth Hospital,University Hospitals Birmingham National Health Service Foundation Trust,Birmingham,United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ye H.","family":"Oo","sequence":"additional","affiliation":[{"name":"Centre for Liver Research, Institute of Immunology and Immunotherapy and National Institute of Health Research Inflammation Biomedical Research Centre Birmingham,University of Birmingham,Birmingham,United Kingdom"},{"name":"Liver Transplantation and Hepatobiliary Unit, Queen Elizabeth Hospital,University Hospitals Birmingham National Health Service Foundation Trust,Birmingham,United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","published-online":{"date-parts":[[2018,2,26]]},"reference":[{"key":"hep41163-bib-0001-20240502","first-page":"827","article-title":"The nature of piecemeal necrosis in chronic active hepatitis","volume":"2","year":"1979","journal-title":"Lancet"},{"key":"hep41163-bib-0002-20240502","doi-asserted-by":"crossref","first-page":"2886","DOI":"10.4049\/jimmunol.0901216","article-title":"Distinct roles for CCR4 and CXCR3 in the recruitment and positioning of regulatory T 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