Role of glycosylation in the H‐2‐restricted cytolysis of virus‐infected cells

Publisher Website
Google Scholar
Abstract
The role of the oligosaccharide portions of cell surface glycoproteins in the susceptibility of virus-infected cells to H-2-restricted cytolysis was investigated by using the antibiotic tunicamycin (TM). TM inhibits the addition of sugars to the polypeptides of glycoproteins. TM treatment of P 815 cells before and during infection with vesicular stomatitis virus (VSV) inhibited glycosylation of proteins and reduced by about 50% the lysis of infected P 815 cells by VSV-immune, H-2-identical killer cells. In contrast, TM treatment had a modest inhibitory effect on cytolysis of P 815 cells by alloimmune effector cells. TM treatment did not inhibit the surface expression of either H-2 or VSV glycoprotein. Thus, glycosylation of H-2 and/or viral glycoprotein is a prerequisite for the lysis of infected cells by H-2-identical, VSV-immune cytotoxic cells.