[Show abstract][Hide abstract] ABSTRACT: Isolated polymorphonuclear leukocytes induce alterations of the antigen receptor mosaic of autologous red cell surfaces in vitro. Such alterations are represented by decreased expression or loss of MN receptors and the ‘appearance’ of HLeb- and Lega-like receptor activities, which can be demonstrated by means of reactions of leukocyte-exposed erythrocytes with anti-H lectins and heterologous anti-Le sera and by specific inhibition of these reactions. Since the receptor changes observed were most pronounced on the surfaces of secretor erythrocytes and since demonstrable Lewis-type modifications could not be created on erythrocytes of nonsecretors in these investigations, the antigenic polymorphism unmasked by contact of red cells with polymorphonuclear leukocytes was genetically limited to some extent. These limitations are perhaps due to restricted antigenic variability of the nonsecretor erythrocyte membrane components. The receptor-modifying activity is confined to particle fractions of polymorphonuclear leukocytes; it is thermostable up to 70 °C, destroyed at 80 °C, blocked by α1 -antitrypsin and other natural protease inhibitors, and reaches its peak at physiological pH values between 7.2 and 7.4. These properties correspond with those of the particulate neutral protease of human polymorphonuclear leukocytes. However, glycosidases probably also play a role.
[Show abstract][Hide abstract] ABSTRACT: Polymorphonuclear leukocytes cause rapid destruction of the blood-group Nhu-receptor on autologous erythrocytes, without the Mhu-receptor activity and the Vicia graminea-receptor activity being simultaneously destroyed. In addition, independently of the original receptor mosaic they create H-specific structures. These particular modifications of specific glycoproteins and the appearance of new receptors sites are considered to be of significance in autologous cell-to-cell interaction.
Full-text · Article · Jun 1972 · European Journal of Immunology