Nonetheless, the intrahepatic immune

response does exist and may be under the regulation of the increase in Treg and in PD1 expression on activated T cells. This observed immune paradox may be of interest for the deciphering of new therapeutic strategies. Disclosures: Juliette Foucher- Board Membership: roche; Speaking and Teaching: BMS, MSD, Gilead Victor de Ledinghen – Advisory Committees or Review Panels: LEE011 ic50 Merck, Janssen, Gilead, Echosens, Boehringer Ingelheim, Abbvie; Grant/Research Support: Roche, Gilead, Janssen; Speaking and Teaching: Roche, Echosens The following people have nothing to disclose: Celine Cognet, Pascale Trimoulet, Julien Vergniol, Wassil Merrouche, Jean francois Moreau, Jean Luc Taupin, Linda Wittkop, Isabelle Pellegrin

Objective: Urokinase plasminogen activator receptor (uPAR) is located on neutrophil cell membranes. The soluble form suPAR is increased in chronic infection by the human immunodeficiency virus and it is predictive of outcome. This prompted us to study the kinetics of suPAR in chronic liver inflammation where no data exist. Methods: suPAR was measured by an enzyme immunoassay in the serum of 28 healthy volunteers and of 275 patients with chronic liver inflammation defined as any more than 2-fold increase of serum aminotransferases for more than six months. Results: Median suPAR were (p values refer to comparisons with healthy controls): 3.51 ng/ml for controls; 6.89 ng/ml for 99 patients with chronic hepatitis B (p< 0.0001); 7.57 ng/ml for 103 patients with chronic hepatitis C (p< Small molecule library 0.0001); 4.71 ng/ml for 29 patients with autoimmune hepatitis (p: 0.004); 3.36 ng/ml for 42 patients with non alcoholic fatty liver disease (NAFLD) (p: 0.606); and 6.89 ng/ml for 3 patients with alcoholic steatohepatitis (p< 0.0001). Using quar-tile distribution, 60 patients with stage of fibrosis between 4 and 6 (Ishak) and belonging to the upper quartile of distribution

were classified with advanced fibrosis. Median suPAR was 6.39 ng/ml in less advanced fibrosis and 8.51 ng/ml in advanced fibrosis respectively (p< 0.0001). After ROC analysis, suPAR greater than 8.98 ng/ml had 90.6% specificity to indicate patients at advanced fibrosis (odds ratio: 上海皓元医药股份有限公司 8.50, 95% CI: 4.23–17.07). A positive correlation was found between serum suPAR and the viral load (rs: +0.271, p: 0.008) and the grade of inflammation (rs: +0.384, p< 0.0001) of HBV patients. No respective correlations were found on HCV patients. Conclusions: suPAR is increased in chronic liver inflammation particularly in fibrosis; Although it can be used as an index of advanced fibrosis, kinetics are largely affected in HBV. Disclosures: The following people have nothing to disclose: Athina Chounta, Vassiliki Tzanetakou, Christakis G.