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Complement receptor 3 (CD11b/CD18) is implicated in the elimination of β‐amyloid peptides
Author(s) -
ChoucairJaafar Nada,
Laporte Vincent,
Levy Rachel,
Poindron Philippe,
Lombard Yves,
Gies JeanPierre
Publication year - 2011
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1111/j.1472-8206.2010.00811.x
Subject(s) - opsonin , phagocytosis , complement receptor , receptor , microglia , integrin alpha m , complement system , macrophage 1 antigen , biology , antibody opsonization , microbiology and biotechnology , biochemistry , chemistry , antibody , immunology , inflammation
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 Aβ 1‐40 or Aβ 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 Aβ 1‐42‐opsonized heat‐killed yeasts and partly in that of Aβ 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.