Abstract
Introduction. The liver is a crucial immunological tolerogenic organ with a unique ability to generate effective immune responses against hepatotropic pathogens while maintaining both local and systemic immune tolerance to self and foreign antigens. Autoimmune hepatitis (AIH) is an immune-mediated inflammatory liver disease caused by the loss of tolerance to liver-specific antigens, leading to autoimmune liver damage.Aim – to summarize current knowledge on the immunopathogenesis of AIH based on information from open sources.Material and methods. The selection of publications was conducted using databases such as PubMed, Clinical Key Elsevier, Cochrane Library, eBook Business Collection, and Google Scholar, which covered information on the immunopathogenesis of AIH. Literature search was performed using keywords: autoimmune diseases, autoimmune hepatitis, Kupffer cells, autoantibodies to liver microsomal antibodies, and mesenchymal stem cells.Research results. Liver immune regulation is mediated by unique cell populations, including T-reg cells, Kupffer cells, and NK cells, which interact to maintain immune tolerance and regulate inflammation. Deficiency or dysfunction of T-reg cells, along with the activation of Th17 cells, contribute to the development of inflammatory processes and autoimmune liver damage. The quantitative and qualitative composition of immune cells in the liver differs significantly from that in secondary lymphoid organs, such as lymph nodes, spleen, or peripheral blood. The CD8+/CD4+ ratio (3.5:1) of liver T cells contrasts with the 1:2 ratio observed in peripheral blood, lymph nodes, and spleen.Conclusions. AIH is a complex disease with a multifaceted immunopathogenesis. T-reg and MSC-based therapies show promising results in clinical trials; however, further research is needed to optimize these methods and ensure their safe and effective application.
Published Version
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