Synergistic action of DPIV and APN in the regulation of T cell function

Adv Exp Med Biol. 2003:524:123-31. doi: 10.1007/0-306-47920-6_16.

Abstract

Inhibitors of the enzymatic activity of alanyl-aminopeptidases severely affect growth and typical functions of human peripheral T cells both in vitro and in vivo. The most prominent changes observed include the activation of cellular signal transduction pathways such as MAP kinases Erk1/2 or the Wnt-pathway, a decrease of production and release of "pro-inflammatory" cytokines (IL-2, IL-12) and, most importantly, an induction of expression and release of the immunosuppressive cytokine, TGF-beta1. Similar effects on T cell proliferation and function have been observed in response to inhibition of DPIV, which is strongly suggestive of a functional synergism of APN and DPIV. In support of this hypothesis evidence is provided showing that the simultaneous application of inhibitors of DPIV and APN further enhances the anti-inflammatory and immunosuppressive effects provoked by the inhibition of APN or DPIV alone. Therefore, the simultaneous inhibition of these enzymes represents a promising strategy for the pharmacological therapy of T cell mediated diseases such as autoimmune disease, inflammation, allergy, and allograft rejection.

MeSH terms

  • Antigens, CD / metabolism
  • CD13 Antigens / metabolism*
  • Cells, Cultured
  • Cytokines / metabolism
  • Dipeptidyl Peptidase 4 / metabolism*
  • Drug Synergism
  • Gene Expression Regulation / immunology
  • Humans
  • Interleukin-2 / genetics*
  • Lymphocyte Activation
  • Reverse Transcriptase Polymerase Chain Reaction
  • T-Lymphocytes / immunology*
  • Transforming Growth Factor beta / genetics*
  • Transforming Growth Factor beta1

Substances

  • Antigens, CD
  • Cytokines
  • Interleukin-2
  • TGFB1 protein, human
  • Transforming Growth Factor beta
  • Transforming Growth Factor beta1
  • CD13 Antigens
  • Dipeptidyl Peptidase 4