{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,25]],"date-time":"2025-09-25T16:38:49Z","timestamp":1758818329106,"version":"3.37.3"},"reference-count":48,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2015,1,22]],"date-time":"2015-01-22T00:00:00Z","timestamp":1421884800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100003042","name":"Else Kr\u00f6ner-Fresenius-Stiftung","doi-asserted-by":"publisher","award":["A47\/2010"],"award-info":[{"award-number":["A47\/2010"]}],"id":[{"id":"10.13039\/501100003042","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Parasite Immunology"],"published-print":{"date-parts":[[2015,2]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>Schistosome infections are renowned for their ability to induce regulatory networks such as regulatory T cells (Treg) that control immune responses against homologous and heterologous antigens such as allergies. However, in the case of co\u2010infections with hepatitis C virus (<jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content>), schistosomes accentuate disease progression and we hypothesized that expanding schistosome\u2010induced Treg populations change their phenotype and could thereby suppress beneficial anti\u2010<jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content> responses. We therefore analysed effector T cells and n\/<jats:styled-content style=\"fixed-case\">iT<\/jats:styled-content>reg subsets applying the markers Granzyme B (GrzB) and Helios in Egyptian cohorts of <jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content> mono\u2010infected (<jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content>), schistosome\u2010co\u2010infected (<jats:italic>Sm<\/jats:italic>\/<jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content>) and infection\u2010free individuals. Interestingly, viral load and liver transaminases were significantly elevated in <jats:italic>Sm<\/jats:italic>\/<jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content> individuals when compared to <jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content> patients. Moreover, overall Treg frequencies and Helios<jats:sup>pos<\/jats:sup>Treg were not elevated in <jats:italic>Sm<\/jats:italic>\/<jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content> individuals, but frequencies of GrzB<jats:sup>+<\/jats:sup>Treg were significantly increased. Simultaneously, GrzB<jats:sup>+<\/jats:sup> <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>8<jats:sup>+<\/jats:sup> T cells were not suppressed in co\u2010infected individuals. This study demonstrates that in <jats:italic>Sm\/<\/jats:italic><jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content> co\u2010infected cohorts, liver disease is aggravated with enhanced virus replication and Treg do not expand but rather change their phenotype with GrzB possibly being a more reliable marker than Helios for <jats:styled-content style=\"fixed-case\">iT<\/jats:styled-content>reg. Therefore, curing concurrent schistosome disease could be an important prerequisite for successful <jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content> treatment as co\u2010infected individuals respond poorly to interferon therapy.<\/jats:p>","DOI":"10.1111\/pim.12171","type":"journal-article","created":{"date-parts":[[2015,1,5]],"date-time":"2015-01-05T08:17:30Z","timestamp":1420445850000},"page":"97-104","source":"Crossref","is-referenced-by-count":12,"title":["Schistosome infection aggravates <scp>HCV<\/scp>\u2010related liver disease and induces changes in the regulatory T\u2010cell phenotype"],"prefix":"10.1111","volume":"37","author":[{"given":"E.","family":"Loffredo\u2010Verde","sequence":"first","affiliation":[{"name":"Institute for Medical Microbiology, Immunology and Hygiene Technische Universit\u00e4t M\u00fcnchen Munich Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"I.","family":"Abdel\u2010Aziz","sequence":"additional","affiliation":[{"name":"Medical Parasitology Kasr Al\u2010Eini University Clinic Cairo Cairo Egypt"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J.","family":"Albrecht","sequence":"additional","affiliation":[{"name":"Institute for Medical Microbiology, Immunology and Hygiene Technische Universit\u00e4t M\u00fcnchen Munich Germany"},{"name":"Clinical Cooperation Group \u2018Immune Monitoring\u2019 Helmholtz Zentrum M\u00fcnchen and Technische Universit\u00e4t M\u00fcnchen Munich Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"N.","family":"El\u2010Guindy","sequence":"additional","affiliation":[{"name":"Clinical &amp; Chemical Pathology Kasr Al\u2010Eini School of Medicine Hospitals Cairo Univeristy Cairo Egypt"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M.","family":"Yacob","sequence":"additional","affiliation":[{"name":"Clinical &amp; Chemical Pathology Kasr Al\u2010Eini School of Medicine Hospitals Cairo Univeristy Cairo Egypt"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A.","family":"Solieman","sequence":"additional","affiliation":[{"name":"Tropical Medicine Departments Kasr Al\u2010Eini School of Medicine Hospitals Cairo Univeristy Cairo Egypt"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"U.","family":"Protzer","sequence":"additional","affiliation":[{"name":"Clinical Cooperation Group \u2018Immune Monitoring\u2019 Helmholtz Zentrum M\u00fcnchen and Technische Universit\u00e4t M\u00fcnchen Munich Germany"},{"name":"Institute of Virology Technische Universit\u00e4t and Helmholtz Zentrum M\u00fcnchen Munich Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"D. 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