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Schistosome infection aggravates HCV ‐related liver disease and induces changes in the regulatory T‐cell phenotype
Author(s) -
LoffredoVerde E.,
AbdelAziz I.,
Albrecht J.,
ElGuindy N.,
Yacob M.,
Solieman A.,
Protzer U.,
Busch D. H.,
Layland L. E.,
Prazeres da Costa C. U.
Publication year - 2015
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/pim.12171
Subject(s) - immunology , biology , hepatitis c virus , cd8 , granzyme b , virology , immune system , phenotype , liver disease , regulatory t cell , hepatitis c , disease , t cell , virus , medicine , il 2 receptor , gene , genetics , biochemistry
Summary 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‐infections with hepatitis C virus ( HCV ), schistosomes accentuate disease progression and we hypothesized that expanding schistosome‐induced Treg populations change their phenotype and could thereby suppress beneficial anti‐ HCV responses. We therefore analysed effector T cells and n/ iT reg subsets applying the markers Granzyme B (GrzB) and Helios in Egyptian cohorts of HCV mono‐infected ( HCV ), schistosome‐co‐infected ( Sm / HCV ) and infection‐free individuals. Interestingly, viral load and liver transaminases were significantly elevated in Sm / HCV individuals when compared to HCV patients. Moreover, overall Treg frequencies and Helios pos Treg were not elevated in Sm / HCV individuals, but frequencies of GrzB + Treg were significantly increased. Simultaneously, GrzB + CD 8 + T cells were not suppressed in co‐infected individuals. This study demonstrates that in Sm/ HCV co‐infected 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 iT reg. Therefore, curing concurrent schistosome disease could be an important prerequisite for successful HCV treatment as co‐infected individuals respond poorly to interferon therapy.