<b>Results:</b> Hepatic accumulation of <sup>18</sup>F-FDG and <sup>18</sup>F-FAC was 173% and 61% higher, respectively, and hepatic accumulation of <sup>18</sup>F-DFA was 41% lower, in a mouse model of autoimmune hepatitis than in control mice.
<b>Results:</b> Hepatic accumulation of <sup>18</sup>F-FDG and <sup>18</sup>F-FAC was 173% and 61% higher, respectively, and hepatic accumulation of <sup>18</sup>F-DFA was 41% lower, in a mouse model of autoimmune hepatitis than in control mice.
Autoimmune hepatitis (AIH) is a chronic liver disease characterized by progressive inflammation, female preponderance and seropositivity for autoantibodies such as anti-smooth muscle actin and/or anti-nuclear, anti-liver kidney microsomal type 1 (anti-LKM1) and anti-liver cytosol type 1 (anti-LC1) in more than 80% of cases.
Autoimmune hepatitis has been associated with polymorphisms of the cytotoxic T lymphocyte antigen-4 gene, reduced hepatic expression of a ligand of programed cell death antigen-1, an interfering soluble variant of this key inhibitory protein, and antibodies against it.
TPMT phenotyping or genotyping may be advisable before institution of azathioprine therapy in AIH but neither approach invariably predicts response to the drug.
PD-L1 and PD-L2 expressions were well correlated with the level of IFN-gamma; however, relatively decreased induction for PD-L1 and PD-L2 by IFN-gamma was observed in AIH or PBC than in CHC.
CTLA4 variations -318C>T and +49A>G were analyzed in 2366 patients with chronic liver disease of various etiologies, including 323 patients with chronic hepatitis B virus (HBV) infection, 1181 patients with chronic hepatitis C virus infection, 180 patients with primary biliary cirrhosis, and 127 patients with autoimmune hepatitis, as well as 202 healthy control individuals.
Glutathione S-transferase (GST) T1 genotype mismatches between donor and recipient have also been suggested to constitute a risk factor for de novo AIH.