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Reversible binding of sialidase-treated rat lymphocytes by homologous peritoneal macrophages
After sialidase treatment, lymphocytes disappear from the blood stream, but reappear after a few hours. The behavior of sialidase-treated rat lymphocytes was investigated by in vitro binding studies with homologous peritoneal macrophages. A lymphocyte mixture from thymus and spleen was treated with sialidase and cultured up to 55 h, and at various times, the binding of the lymphocytes to glass-adherent macrophages was studied by light and electron microscopy; vital lymphocytes were only bound but not phagocytosed, and the interaction with macrophages was inhibited by D-galactose. During culture of lymphocytes, either separately or with macrophages, the binding was more and more reduced, and a second sialidase treatment of cultured lymphocytes led again to increased binding which could be inhibited by D-galactose. This change did not occur in the presence of N-acetyl-2,3-didehydro-2-deoxyneuraminic acid, an inhibitor of sialidases, showing the sialic acid specificity of this phenomenon. Thus, the reversibility of lymphocyte binding could be explained by resynthesis of cell surface sialic acids.
After sialidase treatment, lymphocytes disappear from the blood stream, but reappear after a few hours. The behavior of sialidase-treated rat lymphocytes was investigated by in vitro binding studies with homologous peritoneal macrophages. A lymphocyte mixture from thymus and spleen was treated with sialidase and cultured up to 55 h, and at various times, the binding of the lymphocytes to glass-adherent macrophages was studied by light and electron microscopy; vital lymphocytes were only bound but not phagocytosed, and the interaction with macrophages was inhibited by D-galactose. During culture of lymphocytes, either separately or with macrophages, the binding was more and more reduced, and a second sialidase treatment of cultured lymphocytes led again to increased binding which could be inhibited by D-galactose. This change did not occur in the presence of N-acetyl-2,3-didehydro-2-deoxyneuraminic acid, an inhibitor of sialidases, showing the sialic acid specificity of this phenomenon. Thus, the reversibility of lymphocyte binding could be explained by resynthesis of cell surface sialic acids.