Selectins and mechanisms of signal transduction

J Leukoc Biol. 1998 Jan;63(1):1-14.

Abstract

Leukocyte emigration is essential in both lymphocyte homing, as a central part of immune surveillance, and in leukocyte invasion at sites of inflammation. The emigration of leukocytes requires the interplay of adhesion molecules of the selectin and integrin families and chemokines. Selectin-dependent cell-cell interaction is essential in localizing leukocytes within tissues by promoting the rolling of leukocytes along the endothelial cell surface before development of tight adhesion and subsequent transendothelial migration. Selectins also play an active role in the initiation of intracellular signaling pathways and regulation of cell-cell interactions involving monocytes, lymphocytes, platelets, and endothelial cells. This review focuses mainly on the emerging evidence of biochemical signaling mechanisms involved in the regulation of selectin-dependent leukocyte activation and adhesion, as well as the critical role played by selectins as leukocyte stimulatory molecules. This evidence has serious implications regarding the development of immune and inflammatory responses. This article will also review key structural features of the selectin receptors. A summary is provided of our current understanding of the specific molecular interaction occurring between these adhesion molecules and their counter-receptors, focusing on the critical roles they may play in the regulation of functional responses.

Publication types

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

MeSH terms

  • Animals
  • Cell Membrane / physiology
  • GTP-Binding Proteins / physiology
  • Humans
  • Integrins / physiology
  • Leukocytes / physiology*
  • Ligands
  • Neutrophil Activation
  • Phosphoproteins / physiology
  • Protein-Tyrosine Kinases / physiology
  • Selectins / physiology*
  • Signal Transduction*

Substances

  • Integrins
  • Ligands
  • Phosphoproteins
  • Selectins
  • Protein-Tyrosine Kinases
  • GTP-Binding Proteins