N-acetylglucosaminyltransferase V-deficiency increases susceptibility to murine malaria.

Abstract It is considered that several glycoproteins on erythrocytes in mammalian species are involved in malaria parasite infection. To elucidate the role of N -glycans on malaria parasite infection, we induced experimental murine malaria infection (using Plasmodium berghei ANKA) in mice deficient in N -acetylglucosaminyltransferase V (Mgat5), which is one of the enzymes involved in β1,6-GlcNAc N -glycan biosynthesis. After infection, Mgat5 -/- mice showed severe body weight loss and parasitemia compared with wild-type mice. The Mgat5 -/- mice, but not wild-type mice, also showed severe pathology accompanied by marked infiltration of plasma cells into the lungs and liver. These results suggest that β1,6-GlcNAc N -glycans on/in host erythrocytes may interfere with invasion of the parasites and progression to severe malaria.