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

Authors
  • Loffredo-Verde, E1
  • Abdel-Aziz, I
  • Albrecht, J
  • El-Guindy, N
  • Yacob, M
  • Solieman, A
  • Protzer, U
  • Busch, D H
  • Layland, L E
  • Prazeres da Costa, C U
  • 1 Institute for Medical Microbiology, Immunology and Hygiene, Technische Universität München, Munich, Germany. , (Germany)
Type
Published Article
Journal
Parasite immunology
Publication Date
Feb 01, 2015
Volume
37
Issue
2
Pages
97–104
Identifiers
DOI: 10.1111/pim.12171
PMID: 25559085
Source
Medline
Keywords
License
Unknown

Abstract

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 Helios(pos) Treg 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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