Investigation of the relationship of tissue-resident γδ T cells and IL-17 gene expression with the pathogenesis of autoimmune hepatitis.

Autoimmune hepatitis (AIH) is a chronic inflammatory liver disease. Elevated serum immunoglobulin G (IgG) levels, autoantibodies, and histopathological interface hepatitis are the hallmarks of AIH. Autoantibodies and pathological findings, clinical and biochemical features, typical immunoglobulin levels, and exclusion of other diseases are used to diagnose the condition. Gamma-delta (γδ) T cells are a unique population of unconventional T cells with γ and δ glycoprotein chains. γδ T cells have been shown to play a crucial role in autoimmune diseases by producing interleukin (IL)-17. However, its role in AIH remains to be further elucidated. In this study, we aimed to examine the role of γδ T cells and IL-17 in the pathogenesis of AIH, by working on biopsy samples. Paraffin blocks of 18 patients with type 1 AIH and 18 control liver tissues were analyzed. qRT-PCR assessed IL-17 gene expression. Immunofluorescence double staining of CD3 ⁺ TCRγδ ⁺ was performed to reveal tissue-resident γδ T cells' role in AIH. When comparing AIH to the control, there was a substantial increase in the ratio of CD3 ⁺ TCRγδ ⁺ cells in total inflammatory cells (p = 0.01). IL-17 gene expression was lowered in AIH when compared to the control (p = 0.01). This study provides evidence for the involvement of γδ T cells and IL-17 in the pathogenesis of AIH. The ratio of γδ T cells and IL-17 gene expression showed a significant difference in AIH suggesting a potential role for γδ T cells in driving liver inflammation in A fIH.
Competing Interests: Declarations Ethical approval This study was approved by the Ethical Committee of Kartal Dr. Lutfi Kirdar City Hospital (Ethics No: 2022/514/236/9), School of Medicine, University of Health Sciences, Istanbul, Turkey. Informed consent None Consent to participate The participants have already given informed consent. Consent for publication All authors provide this consent. Conflict of interest The authors declare no competing interests.
(© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)