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Blood, Vol. 95 No. 6 (March 15), 2000:
pp. 2157-2163
Scavenger receptors on liver Kupffer cells mediate the in vivo
uptake of oxidatively damaged red blood cells in mice
Valeska Terpstra and
Theo J. C. van Berkel
From the Division of Biopharmaceutics, Leiden/Amsterdam Center
for Drug Research, University of Leiden, Sylvius Laboratories, Leiden,
The Netherlands.
In vitro studies have shown that damaged red cells and apoptotic
cells are efficiently phagocytosed by scavenger receptors from
macrophages, even under non-opsonizing conditions. Damaged red blood
cells are in vivo effectively removed from the blood circulation, but
the responsible receptor systems are largely unknown. We used a murine
model in which 51Cr-labeled oxidized red blood cells were
injected intravenously, and the cellular uptake sites and the potential
involvement of scavenger receptors were analyzed. The decay of damaged
red cells was rapid (more than 50% removed within 10 minutes after
injection), whereas native red cells were not cleared. The main site of
uptake of damaged red cells was the liver Kupffer cells, which
contained 24% of the injected dose at 10 minutes after injection. The
blood decay and liver uptake were inhibited by typical ligands for
scavenger receptors, such as polyinosinic acid, liposomes containing
phosphatidylserine, oxidized low-density lipoprotein, and
fucoidan, but not by polyadenosinic acid or liposomes without
phosphatidylserine. Mice lacking scavenger receptors class A
type I and II showed no significant decrease in the ability to take up
damaged red cells from the circulation. We conclude that Kupffer cells
are mainly responsible for the removal of damaged red cells from the
blood circulation, a process mediated by polyinosinic acid- and
phosphatidylserine-sensitive scavenger receptors, different from
scavenger receptor class A type I and II. Our data indicate that
scavenger receptors, as pattern-recognizing receptors, play an
important role in vivo in the removal of apoptotic, damaged, or other
unwanted cells from the blood circulation.
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