title: The role of IL-28, IFN-γ, and TNF-α in predicting response to pegylated interferon/ribavirin in chronic HCV patients.
abstract: The primary goal of HCV therapy is to achieve a sustained virological response (SVR). Many host and viral factors influence the treatment response. Cytokines play an important role in the defense against viral infections, where successful treatment of hepatitis C depends on a complex balance between pro- and anti-inflammatory responses. In the present study, we investigated the relationship between the presence and percentage of some cytokines (IL-28, IFN-γ, and TNF-α) regarding different clinicopathological parameters including response to therapy in chronic HCV patients using immunohistochemical technique. This study was carried out on 64 chronic HCV patients (34 responders and 30 non-responders). Of cases, 54% showed IL-28 expression, which was associated with low AST (p = 0.002) and low HAI score (p = 0.006). Of cases, 67 and 45% showed IFN-γ and TNF-α expression, respectively, where the median percentage of TNF-α expression was higher in grade II spotty necrosis compared to grade I. Some inflammatory cytokines expressed by intrahepatic inflammatory cells in chronic HCV patients promote inflammation and injury (pro-inflammatory) such as TNF-α. Other cytokines aid in resolving inflammation and injury (anti-inflammatory) such as IL-28. The balance between these cytokines will determine the degree of inflammatory state. None of the investigated cytokines proved its clear cut role in affecting response to therapy, however, their levels varied between responders and non-responders for further investigations to clarify.
authors.affiliation: Department of Pathology, Faculty of Medicine, Menofiya University, Shebein Elkom, Egypt.
authors.forename: Asmaa Gaber
authors.initials: AG
authors.lastname: Abdou
authors.forename: Nancy Youssef
authors.initials: NY
authors.lastname: Asaad
authors.forename: Nermin
authors.initials: N
authors.lastname: Ehsan
authors.forename: Mohammad
authors.initials: M
authors.lastname: Eltahmody
authors.forename: Maha Mohamed
authors.initials: MM
authors.lastname: El-Sabaawy
authors.forename: Shimaa
authors.initials: S
authors.lastname: Elkholy
authors.forename: Nada Farag
authors.initials: NF
authors.lastname: Elnaidany
mesh_terms: D000328:Adult; D000410:Alanine Transaminase / Q000097:blood; D001219:Aspartate Aminotransferases / Q000097:blood; D015415:Biomarkers / Q000097:blood; D004359:Drug Therapy, Combination; D005260:Female; D016174:Hepacivirus / Q000276:immunology*; D019698:Hepatitis C, Chronic / Q000097:blood / Q000188:drug therapy* / Q000276:immunology / Q000821:virology; D006801:Humans; D007150:Immunohistochemistry; D016898:Interferon-alpha / Q000627:therapeutic use*; D007371:Interferon-gamma / Q000097:blood*; D007378:Interleukins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D011092:Polyethylene Glycols / Q000627:therapeutic use*; D011994:Recombinant Proteins / Q000627:therapeutic use; D012189:Retrospective Studies; D012254:Ribavirin / Q000627:therapeutic use*; D018709:Statistics, Nonparametric; D014409:Tumor Necrosis Factor-alpha / Q000097:blood*; D055815:Young Adult; D000095022:Interferon Lambda
chemical_list: D000410:Alanine Transaminase; D001219:Aspartate Aminotransferases; D015415:Biomarkers; D016898:Interferon-alpha; D007371:Interferon-gamma; D007378:Interleukins; D011092:Polyethylene Glycols; D011994:Recombinant Proteins; D012254:Ribavirin; D014409:Tumor Necrosis Factor-alpha; C000624353:interferon-lambda, human; D000095022:Interferon Lambda; C100416:peginterferon alfa-2a
keywords: IFNγ; IL-28; TNF-α; chronic HCV; immunohistochemistry; pegylated interferon/ribavirin; response to therapy