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2 Integrins1
*
Center for Inflammation Research, Department of Clinical and Surgical Sciences (Internal Medicine), Royal Infirmary, Edinburgh, Scotland;
Infectious Diseases Division, Washington University School of Medicine, St Louis, MO 63110; and
Department of Pathology, Harvard Medical School, Brigham and Women’s Hospital, Boston, MA 02115
Neutrophils undergo constitutive death by apoptosis, leading to
safe nonphlogistic phagocytosis and clearance by macrophages. Recent
work has shown that before secondary necrosis, neutrophils exhibiting
classical features of apoptosis can progress to a morphologically
defined late apoptotic state. However, whether such neutrophils could
be safely cleared was unknown. We now report that human late apoptotic
neutrophils could be purified from cultured neutrophil populations
undergoing constitutive death and were subsequently ingested by human
monocyte-derived macrophages by serum-independent mechanisms that did
not trigger the release of IL-8 or TNF-
. Such ingestion was
specifically inhibited by Abs to thrombospondin-1 and the
v
3 vitronectin receptor. Murine bone
marrow-derived macrophage phagocytosis of late and early apoptotic
neutrophils occurred by similar mechanisms, proceeding with the same
efficiency as that observed for wild-type controls when macrophages
from m-/- or
2-/- mice were used. We conclude that
specific nonphlogistic, 2 integrin-independent
mechanisms involving thrombospondin-1 and
v3 allow macrophages to ingest late
apoptotic neutrophils without eliciting inflammatory cytokine
secretion.
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