Lymphocyte function-associated antigen 1 dominates very late antigen 4 in binding of activated T cells to endothelium

J Exp Med. 1993 Jan 1;177(1):185-90. doi: 10.1084/jem.177.1.185.

Abstract

Lymphocyte function-associated antigen 1/intercellular adhesion molecule 1 (LFA-1/ICAM-1)-and very late antigen 4/vascular cell adhesion molecule 1 (VLA-4/VCAM-1)-mediated adhesion of T lymphocytes to endothelial cells (EC) can be regulated by increased expression of ICAM-1 and VCAM-1 upon cytokine treatment of EC, or by activation of the integrin molecules LFA-1 and VLA-4 on T cells. Here, we provide evidence that preferential usage of LFA-1 over VLA-4 is yet another mechanism to control T cell adhesion. We observed that binding of activated T lymphocytes, as opposed to resting T cells, to EC is essentially mediated through LFA-1 and not through VLA-4. VLA-4-mediated adhesion of T cells to EC is only found when LFA-1 is not expressed or not functional, as observed for several T cell leukemia cell lines. These results suggest that LFA-1-mediated adhesion dominates and may downregulate VLA-4-mediated adhesion through an unidentified mechanism.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Adhesion
  • Cell Adhesion Molecules / physiology
  • Endothelium, Vascular / physiology*
  • Humans
  • Intercellular Adhesion Molecule-1
  • Lymphocyte Activation*
  • Lymphocyte Function-Associated Antigen-1 / physiology*
  • Mice
  • Receptors, Very Late Antigen / physiology*
  • T-Lymphocytes / physiology*
  • Vascular Cell Adhesion Molecule-1

Substances

  • Cell Adhesion Molecules
  • Lymphocyte Function-Associated Antigen-1
  • Receptors, Very Late Antigen
  • Vascular Cell Adhesion Molecule-1
  • Intercellular Adhesion Molecule-1