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The concanavalin A (Con A)-induced liver injury mouse model is a typical animal model focusing on T cell-dependent hepatic damage in the field of autoimmune hepatitis (AIH). However, the underlying mechanism of hepatic dysfunction due to cell activation or signaling pathways triggered by Con A has not been fully clarified. Therefore, the controversy on this model remains in the academic community. In this article, we first summarized the merit and demerit of this contentious model from the perspectives of cell dysfunction, microcirculation disturbance, involved signaling pathways, as well as the properties of Con A. Then, we summed up the scientific implications of the model in elucidating the pathogenesis of AIH, and the shortcomings of this model were also summarized to elucidate the pathogenesis and application prospect of this classical liver injury mouse model in the study of AIH.

The break of immune tolerance and transition from acute to chronic information in the liver lead to the development and persistence of autoimmune hepatitis. Elevated CD279 expression has been detected in type 1 autoimmune hepatitis (AIH) patients with anti‐nuclear and/or anti‐smooth muscle antibodies. This is correlated with increased CD185 positive CD4+ helper T cells which activate B cells producing autoantibodies. However, detailed CD279 profiles on T cell subsets were not clear. Here, we analysed PBMCs of 53 AIH patients and 18 healthy donors. Our work revealed that for their central and effector memory compartment of CD4 T cells was markedly increased. Furthermore, the percentage of CD279+CD185+ and CD279−CD185+ T follicular helper cells as well as CD279+CD185− but not CD279−CD185− populations are significantly enlarged in naïve, central and effector memory subsets. This study suggests that high levels of CD279 and CD185 expression are strongly associated with AIH and may inform disease progression and provide a potential novel therapeutic target. [ABSTRACT FROM AUTHOR]