Complement receptor 3 (CD11b/CD18) is implicated in the elimination of β-amyloid peptides
Nada Choucair-Jaafar1, Vincent Laporte, Rachel Levy
1UMR 7213, Université de Strasbourg, CNRS, 74 route du Rhin, 67401 Illkirch, France. choucair@neurochem.u-strasbg.fr
Abstract:
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.
Related Concept Videos
Complement System
Phagocytosis of Apoptotic Cells
Normal cells contain receptors that prevent them from being recognized by phagocytes.
Receptor Downregulation in MVBs
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR activation may...


