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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Gutkowski, K., Gutkowska, D., Kiszka, J., Partyka, M., Kacperek-Hartleb, T., Kajor, M., & Hartleb, M. (2018). Serum interleukin-17 levels predict inflammatory activity in patients with autoimmune hepatitis. Polish Archives of Internal Medicine, 128(3), 150–156. https://doi.org/10.20452/pamw.4188
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