The anti-inflammatory action of methotrexate is not mediated by lymphocyte apoptosis, but by the suppression of activation and adhesion molecules

Clin Immunol. 2005 Feb;114(2):154-63. doi: 10.1016/j.clim.2004.09.001.

Abstract

Low-dose methotrexate (MTX) is an established and highly effective treatment for severe psoriasis and rheumatoid arthritis; however, its mechanism of action remains unclear. We investigated the effects of low-dose MTX on antigen-stimulated peripheral blood mononuclear cells and explored through which cellular pathways these effects are mediated. We show that MTX caused a dose-dependent suppression of T cell activation and adhesion molecule expression, and this was not due to lymphocyte apoptosis. The suppression of intercellular adhesion molecule (ICAM)-1 was adenosine and folate-dependent, while MTX suppression of the skin-homing cutaneous lymphocyte-associated antigen (CLA) was adenosine-independent. The effect of MTX on CLA, but not ICAM-1, required the constant presence of MTX in cultures. Thus, the suppression of T cell activation and T cell adhesion molecule expression, rather than apoptosis, mediated in part by adenosine or polyglutamated MTX or both, are important mechanisms in the anti-inflammatory action of MTX.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine / pharmacology
  • Anti-Inflammatory Agents / pharmacology*
  • Antigens, Bacterial / immunology
  • Antigens, Differentiation, T-Lymphocyte
  • Antigens, Neoplasm
  • Apoptosis / drug effects
  • Apoptosis / immunology
  • Cell Adhesion Molecules / antagonists & inhibitors*
  • Cell Adhesion Molecules / immunology
  • Flow Cytometry
  • Fucosyltransferases / biosynthesis
  • Fucosyltransferases / genetics
  • Humans
  • Integrins / immunology
  • Intercellular Adhesion Molecule-1 / genetics
  • Intercellular Adhesion Molecule-1 / immunology
  • Leucovorin / pharmacology
  • Lymphocyte Activation / drug effects
  • Lymphocyte Activation / immunology
  • Membrane Glycoproteins / genetics
  • Membrane Glycoproteins / immunology
  • Methotrexate / pharmacology*
  • RNA / chemistry
  • RNA / genetics
  • RNA, Messenger / biosynthesis
  • RNA, Messenger / genetics
  • Receptors, Interleukin-2 / antagonists & inhibitors
  • Receptors, Interleukin-2 / immunology
  • Reverse Transcriptase Polymerase Chain Reaction
  • Streptococcus pyogenes / immunology
  • T-Lymphocytes / cytology
  • T-Lymphocytes / drug effects*
  • T-Lymphocytes / immunology

Substances

  • Anti-Inflammatory Agents
  • Antigens, Bacterial
  • Antigens, Differentiation, T-Lymphocyte
  • Antigens, Neoplasm
  • CTAGE1 protein, human
  • Cell Adhesion Molecules
  • Integrins
  • Membrane Glycoproteins
  • P-selectin ligand protein
  • RNA, Messenger
  • Receptors, Interleukin-2
  • Intercellular Adhesion Molecule-1
  • RNA
  • Fucosyltransferases
  • galactoside 3-fucosyltransferase
  • Adenosine
  • Leucovorin
  • Methotrexate