Mini‐review: A pivotal role for innate immunity in the clearance of apoptotic cells

Apoptotic cells can be recognized and taken up by both macrophages and dendritic cells. Phagocytosis of apoptotic cells generally leads to active suppression of cytokine production by professional phagocytes. This is different from the response towards cells that die by necrosis, which induce a pro‐...

Full description

Saved in:
Bibliographic Details
Published in:European journal of immunology Vol. 34; no. 4; pp. 921 - 929
Main Authors: Roos, Anja, Xu, Wei, Castellano, Giuseppe, Nauta, Alma J., Garred, Peter, Daha, Mohamed R., van Kooten, Cees
Format: Journal Article
Language:English
Published: Weinheim WILEY‐VCH Verlag 01-04-2004
Subjects:
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Apoptotic cells can be recognized and taken up by both macrophages and dendritic cells. Phagocytosis of apoptotic cells generally leads to active suppression of cytokine production by professional phagocytes. This is different from the response towards cells that die by necrosis, which induce a pro‐inflammatory cytokine profile. Uptake of apoptotic cells involves a large number of receptors and opsonins, which bind to cellular ligands exposed during the various stages of apoptotic cell death. Among the opsonins of apoptotic cells, complement factors, including C1q, and complement‐activating members of the pentraxin family play an important role. This is indicated by in vitro phagocytosis studies and supported by the susceptibility to systemic autoimmunity of carriersof genetic deficiencies for early complement proteins. The present review summarizes the role of molecules of innate immunity in the handling of apoptotic cells by macrophages and dendritic cells. It is proposed that C1q and other opsonins prevent autoimmunity and maintain self‐tolerance by supporting the efficient clearance of apoptotic material, as well as by actively modulating phagocyte function.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-1
content type line 23
ObjectType-Feature-3
ObjectType-Review-1
ISSN:0014-2980
1521-4141
DOI:10.1002/eji.200424904