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Association of Treg and TH17 Cytokines with HCV Pathogenesis and Liver Pathology

مؤلف البحث
Amal A Elkhawaga 1, Amal Hosni 2, Doaa Z Zaky 3, Amira A Kamel 4, Nahed A Mohamed 4, Mohamed A Abozaid 5, Muhammad A El-Masry 5
مجلة البحث
Egyptian journal of immunology
المشارك في البحث
الناشر
Egyptian Association of Immunologists.
تصنيف البحث
1
عدد البحث
.Egyptian Volume 28 / No.3 / July 2019 Online ISSN: 2537-0979
موقع البحث
https://pubmed.ncbi.nlm.nih.gov/31926495/
سنة البحث
2019
صفحات البحث
55-63.
ملخص البحث

Chronic hepatitis C (CHC) infection is considered a high risk for development of end-stage liver diseases, particularly server hepatitis, decompensated liver cirrhosis, and hepatocellular carcinoma. Regulatory T cells (Treg) and T-helper 17 (TH17) associated cytokines presumed to play a pivotal role in the immune pathogenesis of HCV infection and stimulate autoimmune diseases. Herein, we tried to assess the association of Treg and TH 17 cytokines with HCV pathogenesis and liver pathology. Fifty CHC infected patients and twenty HCV free controls were included in this study, IL17, IL21, IL10, IL4, TGF- and IL35 serum levels were assessed in both groups using enzyme linked immunosorbent assay (ELISA). CHC infected patients had statistically significant higher values of all serum cytokine levels when compared to the control group (P < 0.0001) for each. Additionally, serum levels of IL17, IL10 and IL35 were positively correlated with viral load. Also, the serum level of IL17 IL21, IL10 and IL35 was positively correlated with ALT serum levels. Only IL21 and IL10 were positively correlated with AST levels. Serum IL17, IL10, TGF- and IL35 levels were significantly elevated in CHC patients with advanced fibrosis stages. We concluded that CHC infected patients displayed high serum levels of Treg and TH17 associated cytokines. Collectively, these results support the hypothesis that liver damage in CHC infection might be due to an immune-mediated destructive mechanism rather than to the direct cytopathic effect of the virus itself.