Aim of the study: Autoimmune hepatitis (AIH) is characterized histologically by aggressive inflammation with
interface hepatitis and prominent lymphoplasmacytic infiltration. Programmed death-1 (PD-1) is expressed on
activated lymphocytes. Engagement of PD-1 by its ligand PD-L1 leads to cell apoptosis and death. We aimed
to evaluate the immunohistochemical expression of PD-1 and PD-L1 in children with AIH, and its relation to
treatment outcome.
Material and methods: Pre-treatment liver biopsies of 31 children with AIH were compared to 30 children with
chronic hepatitis C virus (HCV) infection as a control group. PD-1 was evaluated in lymphocytes, while PD-L1 was
evaluated in lymphocytes, hepatocytes, biliary epithelial cells, sinusoidal endothelial cells and Kupffer cells. All
AIH patients received the standard treatment.
Results: The mean PD-1 was significantly higher in AIH than HCV patients (29.19 ±18.5% vs. 15.2 ±10.1%;
p = 0.002) while there was no statistically significant difference as regards PD-L1 on lymphocytes (p = 0.853).
Neither PD-1 nor PD-L1 correlated with either liver fibrosis or the inflammatory activity (p > 0.05 for all). PD-1/
PD-L1 ratio was significantly higher in AIH compared to HCV patients and in non-responder AIH patients compared
to responders (46.9 vs. 6.58). PD-1 expression was comparable in both responders and non-responders
(p = 0.813), while PD-L1 was significantly upregulated in responders (4.17 ±3.15% vs. 0.63 ±1.3%; p = 0.046).
PD-L1 expression on hepatocytes, biliary epithelial cells, sinusoidal endothelial cells and Kupffer cells was comparable
in AIH and HCV groups.
Conclusions: PD-1/PD-L1 ratio, which reflects immune aggression, was significantly higher in AIH compared to
HCV patients and in non-responder AIH patients compared to responders. |
