Urokinase receptor (uPAR) regulates complement receptor 3 (CR3)-mediated neutrophil phagocytosis

Biochem Biophys Res Commun. 2010 Jun 25;397(2):277-82. doi: 10.1016/j.bbrc.2010.05.100. Epub 2010 May 24.

Abstract

Urokinase receptor (uPAR) associates in cis with complement receptor 3 (CR3). In the present study, we addressed whether this coupling regulates CR3-mediated phagocytosis. CR3-mediated attachment of iC3b-opsonized sheep red blood cells to human neutrophils and internalization of these cells were reduced by removal of cell-bound uPAR by phosphatidylinositol-specific phospholipase C and reconstituted in the presence of soluble uPAR. The attachment and internalization were suppressed in the presence of anti-uPAR polyclonal antibody, proteolytically inactive urokinase and saccharides that disrupt interaction of uPAR with CR3. Thus, uPAR acts as a cofactor for iC3b binding to CR3 and regulates CR3-mediated phagocytosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Membrane / metabolism
  • Complement C3b / metabolism*
  • Humans
  • Macrophage-1 Antigen / metabolism*
  • Neutrophils / immunology*
  • Phagocytosis*
  • Receptors, Urokinase Plasminogen Activator / metabolism*

Substances

  • Macrophage-1 Antigen
  • Receptors, Urokinase Plasminogen Activator
  • Complement C3b