Objectives: Autoimmune hepatitis (AIH) is an aberrant autoimmune condition mediated by T cell abnormality, which may cause fulminant liver failure and persistent liver injury. This study aimed to disclose the histopathological and functional engagement of interleukin (IL)-26, a potent inflammation mediator, in AIH disease progression. Methods: We conducted immunohistochemical staining on liver biopsy samples to evaluate intrahepatic expression of IL-26. Cellular sources of hepatic IL-26 were detected by confocal microscopy. Flow cytometry was employed to determine the immunological alterations of CD4 + and CD8 + T cells following in vitro IL-26 treatment on primary peripheral blood mononuclear cells from healthy controls. Results: Statistically significant increase in IL-26 level was observed in AIH (n = 48) liver samples in comparison with patients having chronic hepatitis B (n = 25), nonalcoholic fatty liver disease (n = 18), and healthy donors for living donor liver transplantation (n = 10). The number of intrahepatic IL-26 + cells was positively correlated with histological and serological severity. An immunofluorescence staining indicated that liver-infiltrating CD4 + T cells, CD8 + T cells, and CD68 + macrophages orchestrated IL-26 secretion in AIH. Both CD4 + and CD8 + T cells demonstrated effective activation, lytic, and proinflammatory functions upon IL-26 stimulation. Conclusion: We observed elevated IL-26 in AIH liver which promoted T cell activation and cytotoxic capacity, indicating a therapeutic potential of IL-26 intervention in AIH.
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