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Phagocytosis of Plasmodium falciparum-infected human red blood cells by
human monocytes: involvement of immune and nonimmune determinants and
dependence on parasite developmental stage
F Turrini, H Ginsburg, F Bussolino, GP Pescarmona, MV Serra and P Arese
Department of Genetics, Biology, and Medical Chemistry, University of
Torino, Italy.
The stage-dependent phagocytosis of Plasmodium falciparum-infected
erythrocytes (IRBC) opsonized with nonimmune serum has been investigated.
An average of 2.9 red blood cell (RBC) harboring ring- forms (RIRBC) and
7.5 RBC infected with trophozoites (TIRBC) or schizonts (SIRBC) were
ingested per monocyte, in comparison with 0.8 noninfected RBC (NRBC) or 5
RBC oxidatively damaged with diamide. Abrogation of generation of
complement component C3b or blockage of its binding to the phagocyte
inhibited phagocytosis of RIRBC by 78% to 95% and of TIRBC by 25% to 50%.
Blockage of immunoglobulin G (IgG) binding reduced phagocytosis of both
RIRBC and TIRBC nonsignificantly by 14%. Preincubation of monocytes with
phosphatidylserine (PS)-containing liposomes reduced phagocytosis of TIRBC
by 22%, but had little effect on RIRBC. Residual, noncomplement, non-IgG-,
and non-PS-dependent phagocytosis amounted to 6% to 18% of total
phagocytosis in RIRBC and TIRBC, respectively. RIRBC bound 2.5 times more
protein A and 3.1 times more anti-C3c (a stable derivative of C3b)
antibodies, and TIRBC bound 20 times more protein A and 6.8 times more
anti-C3c antibodies than NRBC. Phagocytosis of oxidatively damaged RBC and
RIRBC are similar, whereas a higher portion of phagocytosis appears to be
noncomplement- dependent and PS-suppressible in TIRBC. It is concluded that
RIRBC generate recognition signals similar to those present in oxidatively
damaged or senescent RBC. Extensive membrane modifications in TIRBC produce
additional, hitherto undefined signals that induce much higher and
qualitatively distinct phagocytosis.
Volume 80,
Issue 3,
pp. 801-808,
08/01/1992
Copyright © 1992 by The American Society of Hematology
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