Signaling by vascular cell adhesion molecule-1 (VCAM-1) through VLA-4 promotes CD3-dependent T cell proliferation

Eur J Immunol. 1991 Nov;21(11):2871-5. doi: 10.1002/eji.1830211132.

Abstract

Vascular cell adhesion molecule, VCAM-1, is an adhesion molecule expressed on activated endothelium thought to play a role in leukocyte migration to sites of inflammation. VCAM-1 adheres to leukocytes through the VLA-4 integrin. Recombinant soluble VCAM-1 (rsVCAM) and anti-CD3 mAb OKT3 were utilized to address the role of the VCAM-1/VLA-4 pathway in antigen-dependent T cell activation. Monocyte-depleted T cells proliferated upon exposure to co-immobilized OKT3 and rsVCAM but to neither alone. In contrast, an anti-VLA-4 mAb HP1/2 failed to co-activate with OKT3, despite the fact that both rsVCAM and HP1/2 support T cell adhesion comparably. These data indicate that adhesive function is not sufficient for co-stimulatory activity. They also reveal that VCAM-1 may play a role in regulating T cell immune responses as well as migration in vivo.

MeSH terms

  • Antigens, CD / physiology*
  • Antigens, Differentiation, T-Lymphocyte / physiology*
  • CD3 Complex
  • Cell Adhesion
  • Cell Adhesion Molecules / physiology*
  • Humans
  • In Vitro Techniques
  • Lymphocyte Activation*
  • Receptors, Antigen, T-Cell / physiology*
  • Receptors, Very Late Antigen / physiology*
  • Recombinant Proteins / metabolism
  • Signal Transduction
  • T-Lymphocytes / physiology*
  • Vascular Cell Adhesion Molecule-1

Substances

  • Antigens, CD
  • Antigens, Differentiation, T-Lymphocyte
  • CD3 Complex
  • Cell Adhesion Molecules
  • Receptors, Antigen, T-Cell
  • Receptors, Very Late Antigen
  • Recombinant Proteins
  • Vascular Cell Adhesion Molecule-1