INTRODUCTION The etiology of autoimmune hepatitis (AIH) is unclear, with molecular mimicry between host and viral/drug antigens being the most plausible mechanism initiating the immune cascade that induces hepatocyte injury.… Click to show full abstract
INTRODUCTION The etiology of autoimmune hepatitis (AIH) is unclear, with molecular mimicry between host and viral/drug antigens being the most plausible mechanism initiating the immune cascade that induces hepatocyte injury. Finding a serologic parameter that closely relates to the liver histology would be beneficial for monitoring AIH activity and optimizing treatment. OBJECTIVES We studied serum interleukin (IL)-17 levels and IL‑17 activators (IL‑6 and transforming growth factor β1 [TGF-β1]) in treatment-naive and immunosuppressed patients with AIH. We also analyzed the relationships between these cytokines and histological inflammation scores. PATIENTS AND METHODS A total of 44 patients with confirmed AIH were enrolled to the study (22 treatment-naive patients and 22 patients in clinical remission after at least 3 years of immunosuppression). Liver biopsies were performed, and the histological grading of inflammatory activity was performed by a single pathologist. The control group comprised 30 healthy age- and sex‑matched subjects. Serum IL‑17, IL‑6, and TGF‑β1 levels were measured by a quantitative sandwich enzyme immunoassay. RESULTS Serum IL‑17, IL‑6, and TGF‑β1 levels were higher in treatment-naive patients compared with controls (23.2 pg/ml vs 15.3 pg/ml, P = 0.0001; 5.20 pg/ml vs 1.42 pg/ml, P = 0.0001; and 40.5 ng/ml vs 30.1 ng/ml, P = 0.04; respectively). In treatment-naive patients, serum IL‑17 negatively correlated with hepatic inflammation (r = -0.63, P = 0.01). A reduced serum IL‑17 concentration correlated with an increased TGF‑β1 concentration in patients in clinical remission (r = -0.51, P = 0.03). CONCLUSIONS Serum IL‑17 levels may be a useful parameter for assessing disease activity in patients with AIH.
               
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