Targeted disruption of CD43 gene enhances T lymphocyte adhesion

J Immunol. 1993 Aug 1;151(3):1528-34.

Abstract

CD43 is a major leukocyte surface glycoprotein thought to have important functions for T lymphocyte adhesion and activation. We investigated the function of CD43 by using gene targeting to eliminate CD43 expression in the human T lymphocyte line CEM and then testing their adhesive phenotype. Loss of CD43 expression by the CEM cells enhanced their homotypic adhesion and binding to two distinct ligands, fibronectin and HIV-1 gp120. The enhanced homotypic adhesion was blocked specifically by an anti-beta 1 integrin mAb, and the enhanced binding to fibronectin and gp120 was blocked specifically by anti-beta 1 integrin and anti-CD4 mAb, respectively. Partial reconstitution of CD43 expression in the CD43-negative cells resulted in a corresponding reversion to a less adhesive phenotype. These data suggest that CD43 interferes with T lymphocyte adhesion and that CD43 can regulate lymphocyte adhesion by providing a threshold that must be overcome for cell-cell and cell-ligand interactions to occur.

Publication types

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

MeSH terms

  • Antigens, CD*
  • Cell Adhesion
  • Cell Adhesion Molecules / physiology*
  • Fibronectins / metabolism
  • Genes
  • HIV Envelope Protein gp120 / metabolism
  • Humans
  • In Vitro Techniques
  • Leukosialin
  • Ligands
  • Mutagenesis, Insertional
  • Sialoglycoproteins / physiology*
  • T-Lymphocytes / cytology*

Substances

  • Antigens, CD
  • Cell Adhesion Molecules
  • Fibronectins
  • HIV Envelope Protein gp120
  • Leukosialin
  • Ligands
  • SPN protein, human
  • Sialoglycoproteins