Signaling pathways in phagocytosis

Bioessays. 1999 May;21(5):422-31. doi: 10.1002/(SICI)1521-1878(199905)21:5<422::AID-BIES9>3.0.CO;2-#.

Abstract

Phagocytosis is an uptake of large particles governed by the actin-based cytoskeleton. Binding of particles to specific cell surface receptors is the first step of phagocytosis. In higher Eucaryota, the receptors able to mediate phagocytosis are expressed almost exclusively in macrophages, neutrophils, and monocytes, conferring immunodefence properties to these cells. Receptor clustering is thought to occur upon particle binding, that in turn generates a phagocytic signal. Several pathways of phagocytic signal transduction have been identified, including the activation of tyrosine kinases and (or) serine/threonine kinase C in pivotal roles. Kinase activation leads to phosphorylation of the receptors and other proteins, recruited at the sites of phagocytosis. Monomeric GTPases of the Rho and ARF families are likely to be engaged downstream of activated receptors. The GTPases, in cooperation with phosphatidylinositol 4-phosphate 5-kinase and phosphatidylinositol 3-kinase lipid modifying enzymes, can modulate locally the assembly of the submembranous actin filament system leading to particle internalization.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Actins / physiology
  • Animals
  • Cytoskeleton / physiology
  • GTP Phosphohydrolases / metabolism
  • Humans
  • Phagocytosis*
  • Phosphatidylinositol 3-Kinases / metabolism
  • Phosphotransferases (Alcohol Group Acceptor) / metabolism
  • Protein Kinase C / metabolism
  • Protein-Serine-Threonine Kinases / metabolism
  • Protein-Tyrosine Kinases / metabolism
  • Receptors, Cell Surface / metabolism
  • Signal Transduction*

Substances

  • Actins
  • Receptors, Cell Surface
  • Phosphatidylinositol 3-Kinases
  • Phosphotransferases (Alcohol Group Acceptor)
  • 1-phosphatidylinositol-4-phosphate 5-kinase
  • Protein-Tyrosine Kinases
  • Protein-Serine-Threonine Kinases
  • Protein Kinase C
  • GTP Phosphohydrolases