Selective tyrosine kinase inhibition by imatinib mesylate for the treatment of autoimmune arthritis

J Clin Invest. 2006 Oct;116(10):2633-42. doi: 10.1172/JCI28546. Epub 2006 Sep 14.

Abstract

Tyrosine kinases play a central role in the activation of signal transduction pathways and cellular responses that mediate the pathogenesis of rheumatoid arthritis. Imatinib mesylate (imatinib) is a tyrosine kinase inhibitor developed to treat Bcr/Abl-expressing leukemias and subsequently found to treat c-Kit-expressing gastrointestinal stromal tumors. We demonstrate that imatinib potently prevents and treats murine collagen-induced arthritis (CIA). We further show that micromolar concentrations of imatinib abrogate multiple signal transduction pathways implicated in RA pathogenesis, including mast cell c-Kit signaling and TNF-alpha release, macrophage c-Fms activation and cytokine production, and fibroblast PDGFR signaling and proliferation. In our studies, imatinib attenuated PDGFR signaling in fibroblast-like synoviocytes (FLSs) and TNF-alpha production in synovial fluid mononuclear cells (SFMCs) derived from human RA patients. Imatinib-mediated inhibition of a spectrum of signal transduction pathways and the downstream pathogenic cellular responses may provide a powerful approach to treat RA and other inflammatory diseases.

Publication types

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

MeSH terms

  • Animals
  • Arthritis, Experimental / drug therapy*
  • Arthritis, Experimental / metabolism
  • Arthritis, Experimental / pathology
  • Autoantigens / immunology
  • B-Lymphocytes / drug effects
  • B-Lymphocytes / immunology
  • B-Lymphocytes / metabolism
  • Benzamides
  • Cell Proliferation / drug effects
  • Collagen Type II / immunology
  • Humans
  • Imatinib Mesylate
  • Macrophages, Peritoneal / drug effects
  • Macrophages, Peritoneal / metabolism
  • Male
  • Mast Cells / drug effects
  • Mast Cells / metabolism
  • Mast Cells / pathology
  • Mice
  • Mice, Inbred DBA
  • Mice, Transgenic
  • Phosphorylation / drug effects
  • Piperazines / pharmacology
  • Piperazines / therapeutic use*
  • Protein Kinase Inhibitors / pharmacology
  • Protein Kinase Inhibitors / therapeutic use
  • Protein-Tyrosine Kinases / antagonists & inhibitors*
  • Protein-Tyrosine Kinases / metabolism
  • Proto-Oncogene Proteins c-kit / metabolism
  • Pyrimidines / pharmacology
  • Pyrimidines / therapeutic use*
  • Receptor, Macrophage Colony-Stimulating Factor / metabolism
  • Receptor, Platelet-Derived Growth Factor beta / metabolism
  • Signal Transduction / drug effects
  • Stem Cell Factor / pharmacology
  • Synovial Fluid / cytology
  • Synovial Fluid / drug effects
  • Synovial Fluid / metabolism
  • T-Lymphocytes / drug effects
  • T-Lymphocytes / immunology
  • T-Lymphocytes / metabolism
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Autoantigens
  • Benzamides
  • Collagen Type II
  • Piperazines
  • Protein Kinase Inhibitors
  • Pyrimidines
  • Stem Cell Factor
  • Tumor Necrosis Factor-alpha
  • Imatinib Mesylate
  • Protein-Tyrosine Kinases
  • Proto-Oncogene Proteins c-kit
  • Receptor, Macrophage Colony-Stimulating Factor
  • Receptor, Platelet-Derived Growth Factor beta