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Phagocytosis of phenylhydrazine oxidized and G-6-PD-deficient red blood
cells: the role of cell-bound immunoglobulins
S Horn, N Bashan and J Gopas
Department of Microbiology, Faculty of Health Sciences, Ben-Gurion
University of the Negev, Beer Sheva, Israel.
In this study, the role of Igs in the recognition and removal of
oxidatively damaged human red blood cells (RBCs) was investigated.
Phagocytosis of normal RBCs exposed to the oxidative hemolytic agent
phenylhydrazine (Phz) and of glucose-6-phosphate dehydrogenase (G6PD)-
deficient RBCs by murine macrophages was examined. A 40-fold increase in
phagocytosis of RBCs treated with 3 mmol/L Phz was obtained both in the
absence and presence of autologous serum, indicating that binding of
autologous antibodies to the oxidized cells is not essential for
phagocytosis. Yet, a basal number of IgG molecules was found to be present
on the RBCs, as determined both by binding of 125I protein A and
fluorescein isothiocyanate-antihuman Ig to the cells. Macrophage Fc
receptors were found to be involved in the recognition of the RBCs, because
phagocytosis was partially inhibited by incubating macrophages with bovine
serum albumin (BSA) anti-BSA complexes, aIg (aggregated Igs), and anti-Fc
receptor II monoclonal antibodies. Galactose/mannose inhibited phagocytosis
of oxidized RBCs additively to aIg. Because phagocytosis was decreased when
Phz-RBCs were incubated with F(ab')2 fragments of antihuman antibodies, it
is suggested that the basal amount of Igs bound to the cells plays a role
in the recognition of Phz- RBCs. G6PD-deficient RBCs were recognized and
phagocytosed by murine macrophages without preexposure to oxidants in vitro
(mean of 19 RBCs/100 macrophages). This phagocytosis was not affected by
the addition of serum and was inhibited by incubating macrophages with
galactose/mannose and the various Fc receptor blockers. A positive
correlation between hemoglobin content and the number of cell-bound Igs to
each patient erythrocytes was found. These results support the involvement
of both an Fc and a lectin-like macrophage receptor in the recognition and
phagocytosis of Phz-oxidized and G6PD-deficient RBCs and suggest
opsonization as a possible physiologic process for the removal of severe
damaged RBCs.
Volume 78,
Issue 7,
pp. 1818-1825,
10/01/1991
Copyright © 1991 by The American Society of Hematology
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