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Loffredo-Verde, E.* ; Abdel-Aziz, I.Z.* ; Albrecht, J. ; El Guindy, N.M.* ; Yacob, M.* ; Solieman, A.S.* ; Protzer, U. ; Busch, D.H. ; Layland, L.E.* ; Prazeres da Costa, C.U.*

Schistosome infection aggravates HCV-related liver disease and induces changes in the regulatory T-cell phenotype.

Parasite Immunol. 37, 97-104 (2015)
Verlagsversion DOI PMC
Free by publisher
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
© 2015 John Wiley & Sons Ltd. 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/iTreg 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 HeliosposTreg were not elevated in Sm/HCV individuals, but frequencies of GrzB+Treg were significantly increased. Simultaneously, GrzB+ CD8+ 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 iTreg. Therefore, curing concurrent schistosome disease could be an important prerequisite for successful HCV treatment as co-infected individuals respond poorly to interferon therapy.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Granzyme B ; Helios ; Hepatitis C Virus ; Liver Disease ; Regulatory T Cells ; Schistosoma Mansoni; Hepatitis-c Virus; Helminth Infection; Expression Defines; Immune-responses; Cd127 Expression; Nile Delta; Egypt; Mansoni; Epidemiology; Polarization
ISSN (print) / ISBN 0141-9838
e-ISSN 1365-3024
Zeitschrift Parasite Immunology
Quellenangaben Band: 37, Heft: 2, Seiten: 97-104 Artikelnummer: , Supplement: ,
Verlag Blackwell
Verlagsort Oxford
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Virology (VIRO)
Institute of Molecular Immunology (IMI)