Complement receptor 3 (CD11b/CD18) is implicated in the elimination of β-amyloid peptides

被引：29

作者：

Choucair-Jaafar, Nada ^{[1
]}

Laporte, Vincent ^{[2
]}

Levy, Rachel ^{[1
]}

Poindron, Philippe ^{[1
]}

Lombard, Yves ^{[1
]}

Gies, Jean-Pierre ^{[1
]}

机构：

[1] Univ Strasbourg, CNRS, UMR 7213, F-67401 Illkirch Graffenstaden, France

[2] Catholic Univ Louvain, Inst Neurosci, Expt Pharmacol Unit, B-1200 Brussels, Belgium

来源：

FUNDAMENTAL & CLINICAL PHARMACOLOGY | 2011年 / 25卷 / 01期

关键词：

Alzheimer's disease; antibodies; beta-amyloid peptide; complement receptor; low density lipoprotein receptor-related protein; microglia; phagocytosis; MICROGLIAL CELLS; NEUTROPHIL PHAGOCYTOSIS; MONONUCLEAR PHAGOCYTES; ALZHEIMER; DISEASE; PROTEIN; ACTIVATION; PLAQUES; SYSTEM; BRAIN;

D O I：

10.1111/j.1472-8206.2010.00811.x

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Microglia are the professional phagocytes of the brain and express phagocytic receptors such as complement receptor 3 (CR3 or CD11b/CD18). Using mimics of the amyloid deposit made of heat-killed yeasts coated with either A beta 1-40 or A beta 1-42, we were able to study how microglia interacted with and ingested these particles in vitro. We have shown previously that the low density lipoprotein receptor-related protein (LRP) is largely implied in the phagocytosis of A beta 1-42-opsonized heat-killed yeasts and partly in that of A beta 1-40-opsonized heat-killed yeasts. Here, we report that antibodies against CD11b or CD18 reduced the uptake of the artificial amyloid deposit by microglial cell showing that CR3 is involved in the mechanism. Moreover, a concomitant inhibition of LRP and CR3 completely blocked the ingestion of both kinds of particles suggesting that no other receptors participate to this mechanism.

引用

页码：115 / 122

页数：8

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