Abstract
Autoimmune hepatitis (AIH) is a severe and chronic liver disease, and its incidence has increased worldwide in recent years. Research into the pathogenesis of AIH remains limited largely owing to the lack of suitable mouse models. The concanavalin A (ConA) mouse model is a typical and well-established model used to investigate T cell-dependent liver injury. However, ConA-induced hepatitis is acute and usually disappears after 48 h; thus, it does not mimic the pathogenesis of AIH in the human body. Several studies have explored various AIH mouse models, but as yet there is no widely accepted and valid mouse model for AIH. Immunosuppression is the standard clinical therapy for AIH, but patient side effects and recurrence limit its use. Regulatory T cells (Tregs) play critical roles in the maintenance of immune homeostasis and in the prevention of autoimmune diseases, which may provide a potential therapeutic target for AIH therapy. However, the role of Tregs in AIH has not yet been clarified, partly because of difficulties in diagnosing AIH and in collecting patient samples. In this review, we discuss the studies related to Treg in various AIH mouse models and patients with AIH and provide some novel insights for this research area.
Highlights
Autoimmune hepatitis (AIH) is a progressive inflammatory liver disease characterized by chronic inflammation of the liver, circulating autoantibodies, hypergammaglobulinemia, and specific liver biopsy histologic features [1, 2]
AIH, autoimmune hepatitis; ConA, concanavalin A; S100, syngeneic liver homogenate; TF-OVA mouse, the model antigen ovalbumin is expressed in hepatocytes of the mouse; Traf6 TEC, conditional deletion of tumor necrosis factor receptor-associated factor 6 expression in the thymic epithelial cells; PD-1, programmed cell death protein 1; NTx, neonatal theymectomy; FC, flow cytometry; WB, western blotting; PCR, polymerase chain reaction; IHC, immunohistochemistry
AIH is a chronic and progressive immune-mediated liver disease that can lead to cirrhosis, hepatocellular carcinoma, liver transplantation, and death [135,136,137]
Summary
Autoimmune hepatitis (AIH) is a progressive inflammatory liver disease characterized by chronic inflammation of the liver, circulating autoantibodies, hypergammaglobulinemia, and specific liver biopsy histologic features (interface hepatitis, rosettes, and lymphocyte invasion) [1, 2]. It is widely accepted that both the initiation of the selfattack and the subsequent dysregulation of the immune system in the liver microenvironment contribute to the progressive process of liver damage During this process, helper T (Th) cells play the most important role in triggering this self-attack process by recognizing the autoantigens [29], while B cells are responsible for the subsequent production of autoantibodies [29]. A well-established diagnostic scoring system with acceptable specificity and sensitivity is in use [35], AIH diagnosis remains difficult, largely owing to its dependence on liver biopsy. It is difficult to progress basic research in the area of AIH because of the lack of a suitable and widely accepted mouse model that imitates the AIH disease process in humans
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