This study showed that the direct and indirect effect of IL-37 on macrophages could reduce the hepatic TNF-α expression, and also modulate IL-1β/IL-12 and IL-10/IL-1Ra expression to suppress the hepatic IFN-γ expression, thus suppressing the development of T cell-dependent liver injury such as autoimmune hepatitis.
G/T alleles of IL-2 at -330 (rs2069762) and A/T alleles on UTR +5644 position at IFN-γ and their subsequent haplotypes, did not show significant association with AIH.
Exposure to ISDs contains IFN-γ and PD-1 expression in AIH, where control over CD4<sup>+</sup> CD25<sup>-</sup> cell proliferation is also noted upon exposure to MPA.
In AIH, Gal9(pos) T-regs were fewer and contained less FOXP3(pos), IL-10(pos), and transforming growth factor β(pos) and more IFNγ(pos) and IL-17(pos) cells than HS. siRNA treatment of Gal-9(pos) T-regs drastically reduced T-reg ability to suppress CD4(pos) CD25(neg) and Tim-3(pos) cell proliferation in AIH and HS.
IL-1 beta and interferon gamma mRNA showed increased expression in cirrhotics with autoimmune chronic active hepatitis compared with those with primary biliary cirrhosis.