RED-BLOOD-CELL PHAGOCYTOSIS FOLLOWING HEXOKINASE INACTIVATION

Hexokinase inactivating antibodies were loaded into human erythrocytes using an encapsulation procedure based on hypotonic haemolysis, isoto nic resealing and reannealing. Red blood cells loaded with anti-hexoki nase IgG showed 20 percent residual hexokinase activity and reduced gl ycolytic activity.(9) Incubation of these cells in the presence of an oxidizing agent such as terbutyl hydroperoxide (TBH) and then in autol ogous plasma, promoted opsonization by autologous IgG and complement d eposition, but not haemolysis. Furthermore, the antihexokinase IgG loa ded cells treated with TBH were actively recognized and phagocytosed b y macrophages. Thus, metabolic impairment of human erthrocytes promote s autologous IgG binding, C3 deposition and phagocytosis, a mechanism already reported for the removal of senescent erythrocytes.