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N‑Acetylglucosaminyltransferase V (GnT‑V) catalyzes β1‑6 branching in asparagine‑linked oligosaccharides and is one of the most important glycosyltransferases involved in carcinogenesis, cancer metastasis and immunity. To investigate the biological functions of GnT‑V, the present study developed GnT‑V transgenic (Tg) mice and the role of GnT‑V in experimental immune‑mediated hepatitis, induced by concanavalin A (ConA), were investigated. It was found that the aberrant expression of GnT‑V exacerbated ConA‑induced hepatitis in the Tg mice compared with the wild‑type (WT) mice. The survival rate of the ConA‑induced hepatitis at a high‑dose of ConA was significantly lower in the Tg mice. Intravenously injected ConA is known to initially bind predominantly to the mannose gland of the liver sinusoidal endothelial cell (LSEC) surface and to leads to the activation of various immune cells. In the present study, the binding affinity of ConA to the LSECs did not differ between the WT and Tg mice. In addition, T cell receptor stimulation by anti‑cluster of differentiation (CD)3/CD28 antibodies produced lower levels of T helper (Th)1 cytokine (interferon‑γ) and higher levels of Th2 cytokine (interleukin‑10) in the Tg mouse splenic lymphocytes compared with WT mice. The composition of the hepatic mononuclear cells revealed that CD11b‑positive cells were significantly increased in the GnT‑V Tg mice. In addition, F4/80‑positive cells were significantly increased in the Tg mouse liver and the depletion of macrophages reduced the difference in the severity of ConA‑induced hepatitis between the WT and Tg mice. In conclusion, the present findings indicated that the aberrant expression of GnT‑V led to an increase in hepatic macrophage infiltration and enhanced ConA‑induced hepatitis. Modulation of glycosylation may be a novel therapeutic target for immunity‑associated acute hepatitis.

N-Acetylglucosaminyltransferase V exacerbates concanavalin A-induced hepatitis in mice