Blockade of signaling via the very late antigen (VLA-4) and its counterligand vascular cell adhesion molecule-1 (VCAM-1) causes increased T cell apoptosis in experimental autoimmune neuritis

Acta Neuropathol. 2002 Feb;103(2):131-6. doi: 10.1007/s004010100444. Epub 2001 Oct 31.

Abstract

We characterized the early effects of anti-very late antigen (VLA-4) and its counterligand vascular cell adhesion molecule-1 (VCAM-1) antibody therapy on T cell infiltration and apoptosis in adoptive transfer experimental autoimmune neuritis of female Lewis rats. At the peak of disease, animals were treated with anti-VCAM-1 monoclonal antibody (mAb), anti-VLA-4 mAb, or the respective isotype mAb controls 18, 12, or 6 h before perfusion. Anti-VCAM-1 led to a rapid, significant increase of apoptotic T cells in the sciatic nerve with a maximum after 6 h, preceding the significant decrease of T cell infiltration seen after 18 h. This was accompanied by a significant reduction in mRNA levels for IFN-gamma and inducible nitric oxide synthase. The results for anti-VLA-4 treatment showed a similar trend. The early increase of T cell apoptosis following disruption of VLA-4/VCAM-1 interaction may reflect a novel signaling component of proapoptotic pathways.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Allergic Agents / antagonists & inhibitors*
  • Anti-Allergic Agents / pharmacology*
  • Apoptosis / drug effects*
  • Apoptosis / physiology
  • Disease Models, Animal
  • Disease Progression
  • Female
  • Integrin alpha4beta1
  • Integrins / antagonists & inhibitors*
  • Neuritis, Autoimmune, Experimental / pathology
  • Neuritis, Autoimmune, Experimental / physiopathology*
  • Rats
  • Rats, Inbred Lew
  • Receptors, Lymphocyte Homing / antagonists & inhibitors*
  • Signal Transduction / drug effects*
  • Signal Transduction / physiology
  • T-Lymphocytes / drug effects*
  • T-Lymphocytes / pathology
  • T-Lymphocytes / physiology
  • Time Factors
  • Vascular Cell Adhesion Molecule-1 / pharmacology*

Substances

  • Anti-Allergic Agents
  • Integrin alpha4beta1
  • Integrins
  • Receptors, Lymphocyte Homing
  • Vascular Cell Adhesion Molecule-1