Document Detail


Immunopathological consequences of the loss of engulfment genes: the case of ABCA1.
MedLine Citation:
PMID:  16471259     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Programmed cell death plays a crucial role in the maintenance of cell homeostasis. An initial, effector phase leads to the generation of apoptotic corpses and is closely followed by a swift clearance by professional or amateur phagocytes. Several aspects distinguish this latter process of engulfment of dying cells from the classical forms of phagocytosis. They concern all aspects of the process from the recognition of the prey to the final outcome, i.e. immunological silence. The engulfment of dead cells is a process highly conserved through evolution and it has been studied in parallel in two systems, mammalian cells and the nematode C. elegans. ABCA1 and its ortholog CED-7 in the nematode are key players of engulfment. Their mode of action is somehow original in the panorama of engulfment receptors since they act as lipid transporters. While in the worm the loss of CED-7 has phenotypic consequences exclusively on engulfment, in the mouse the deletion of ABCA1 by homologous recombination has highlighted broad consequences on macrophage biology. Among those we will discuss here the aberrant responses of ABCA1-/- mice to Plasmodium berghei ANKA infection, concerning in particular the development of cerebral malaria (CM), a cytokine-induced immunopathology. This syndrome involves a central role of monocytes and, as shown recently, high levels of circulating microparticles. It was found that ABCA1 loss completely protects against CM and its associated mortality. This observation, together with the demonstration of quantitative and functional modifications of microparticles, suggests that microparticles may be involved in CM pathogenesis. The ABCA1 transporter thus appears to control susceptibility to CM, thereby providing new insights in its pathophysiological mechanisms and potential new therapeutic avenues.
Authors:
Georges E Grau; Giovanna Chimini
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Journal de la Société de biologie     Volume:  199     ISSN:  1295-0661     ISO Abbreviation:  J. Soc. Biol.     Publication Date:  2005  
Date Detail:
Created Date:  2006-02-13     Completed Date:  2006-03-24     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100890617     Medline TA:  J Soc Biol     Country:  France    
Other Details:
Languages:  eng     Pagination:  199-206     Citation Subset:  IM    
Affiliation:
Immunopathology Group, Faculté de Médecine, IFR48, 27, boulevard Jean Moulin, F-13385 Marseille Cedex 5, France.
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MeSH Terms
Descriptor/Qualifier:
ATP-Binding Cassette Transporters / genetics,  physiology*
Animals
Apoptosis / immunology,  physiology*
Autoantigens / immunology
Caenorhabditis elegans Proteins / genetics,  physiology*
Cell Adhesion Molecules / physiology
Cytokines / physiology
Evolution, Molecular
Gene Deletion
Humans
Lipids / physiology
Macrophages / physiology
Malaria, Cerebral / immunology,  pathology*,  physiopathology
Mammals / physiology
Mice
Mice, Inbred DBA
Mice, Knockout
Models, Biological
Monocytes / physiology
Particle Size
Phagocytosis / genetics*,  immunology
Phenotype
Plasmodium berghei
Receptors, Cell Surface / physiology
Chemical
Reg. No./Substance:
0/ATP binding cassette transporter 1; 0/ATP-Binding Cassette Transporters; 0/Autoantigens; 0/CED-7 protein, C elegans; 0/Caenorhabditis elegans Proteins; 0/Cell Adhesion Molecules; 0/Cytokines; 0/Lipids; 0/Receptors, Cell Surface

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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