CD36 is required for phagocytosis of apoptotic cells by human macrophages that use either a phosphatidylserine receptor or the vitronectin receptor (alpha v beta 3).

摘要: In vivo, apoptotic cells are efficiently removed by professional or nonprofessional phagocytes, a process thought to be essential for tissue remodeling and resolution of inflammation. Macrophages recognize several mechanisms, including recognition exposed phosphatidylserine (PS); however, PS on has not been identified as feature human macrophages. The purpose this study was determine whether monocyte-derived macrophages could stimulated PS, defined inhibition phagocytosis PS-containing liposomes. We also assessed the potential roles scavenger receptors, CD14, lectins. Uptake neutrophils into unstimulated blocked about 50% Arg-Gly-Asp-Ser anti-alpha(v), up 20% oxidized low density lipoprotein N-acetylglucosamine, implying major role integrin minor lectin receptors. with beta-1,3-glucan liposomes 40% lipoprotein, suggesting that had switched from using PS. MEM-18 61D3 (anti-CD14 mAbs) were poor inhibitors neutrophil uptake, but good lymphocyte uptake. switch accompanied down-regulation alpha(v)beta3 expression function. Anti-CD36 uptake macrophages, CD36 involvement only mechanism (as previously reported) recognition. A maximum 70% achieved combining anti-CD36 either anti-a(v)