Purified CD4+CD25+ and CD4+CD25- T cells from 24 patients with type 1 AIH and 22 healthy controls were cultured for up to 5 weeks with anti-CD3/anti-CD28 T cell expander and high-dose interleukin-2 (IL-2).
Here we report that the amplified non-AIH liver inflammation could promote the initiation of AIH due to the sustained increase of IL-6, IL-12, IL-4, and IL-25 in the liver.
The haplotype GA of IL-6 at -174 and nt565, was significantly overrepresented in the AIH group, compared to (20.9% of AIH vs. 1.4% in controls p < 0.0001).
Additionally, we typed 117 patients and 227 controls for functional polymorphisms of IL4, IL13, IL5, and IL4RA genes involved in IgE switching and eosinophil maturation that might contribute to overall genetic susceptibility to AIH.
Also, the serum levels of IL-17A and IL-22 were correlated positively with liver injury (ALT/AST), whereas the serum levels of IL-10 were correlated negatively with hypergammaglobulinaemia (IgG, IgM) in AIH patients.
Additionally, we typed 117 patients and 227 controls for functional polymorphisms of IL4, IL13, IL5, and IL4RA genes involved in IgE switching and eosinophil maturation that might contribute to overall genetic susceptibility to AIH.
According to the univariate analysis, overlapping features of autoimmune hepatitis (rPSC in 5/5, <i>P</i> ≤ 0.05) and <i>HLA-DRB1*07</i> in the donor (rPSC in 10/15, <i>P</i> ≤ 0.05) represent other potential risk factors for rPSC, while the <i>HLA-DRB1*04</i> (rPSC in 0/6, <i>P</i> ≤ 0.05), <i>HLA-DQB1*03</i> (rPSC in 1/11, <i>P</i> ≤ 0.05), and <i>HLA-DQB1*07</i> (rPSC in 0/7, <i>P</i> ≤ 0.05) recipient alleles may have protective roles.