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005

DIFFERENTIAL EFFECT OF ANTI-ALPHA4 INTEGRIN AND ANTI-VASCULAR ADHESION PROTEIN-1 ANTIBODIES ON THE CONCANAVALIN A-INDUCED HEPATITIS

WY Lee, P Kubes
Immunology Research Group, Department of Physiology and Biophysics, Faculty of Medicine, University of Calgary, Calgary, Alberta

Hepatitis derived by concanavalin A (Con A) in mice is well known to be a lymphocyte-mediated disease. It has been reported that Th1 and Th2 lymphocytes use alpha4 integrin and vascular adhesion protein (VAP)-1, respectively, to adhere within the hepatic sinusoids. Therefore, we investigated whether the monoclonal antibodies against them can ameliorate the Con A-induced hepatic damage in vivo, and can inhibit the change in the hepatic lymphocyte profile derived by Con A. Saline or antibodies to alpha4 integrin (PS/2, 100 µg) or VAP-1 (cocktail of 7-88 and 7-106, 50 µg each) were administered intravenously 30 min before Con A (13, 15, or 20 mg/kg, i.v.) administration. Con A treatment markedly increased the serum level of alanine aminotransferase (ALT) in a dose-dependent manner. Interestingly, an intermediate dose of Con A (15 mg/kg) induced liver injury was attenuated by anti-VAP-1 antibody, while anti-alpha4 integrin antibody enhanced Con A-induced injury. However, neither antibody affected the increase in ALT level at 24 h after Con A administration. In immunophenotyping analysis using flow cytometry, we observed a massive infiltration of NK and CD3 T cells and a decrease in NKT cells by Con A. Pretreatment with anti-VAP-1 antibodies attenuated the increase in CD3 T cells, but did not influence the NK and NKT cells. Con A treatment increased the number of both CD4 and CD8 T lymphocytes, and pretreatment with anti-VAP-1 antibody prevented the increase of both. Anti-alpha4 integrin antibody did not reduce CD4 or CD8 lymphocyte recruitment into the liver. Our findings suggest that anti-VAP-1 antibody ameliorates the Con A-induced hepatic injury, which is associated with its blocking the infiltration of CD4 and CD8 lymphocytes.
This study was supported by CIHR and the CIHR training program

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