| First Author | Choucair-Jaafar N | Year | 2011 |
| Journal | Fundam Clin Pharmacol | Volume | 25 |
| Issue | 1 | Pages | 115-22 |
| PubMed ID | 20199584 | Mgi Jnum | J:242546 |
| Mgi Id | MGI:5905548 | Doi | 10.1111/j.1472-8206.2010.00811.x |
| Citation | Choucair-Jaafar N, et al. (2011) Complement receptor 3 (CD11b/CD18) is implicated in the elimination of beta-amyloid peptides. Fundam Clin Pharmacol 25(1):115-22 |
| abstractText | 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 Abeta 1-40 or Abeta 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 Abeta 1-42-opsonized heat-killed yeasts and partly in that of Abeta 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. |
