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Dysfunction of endothelial progenitor cells is associated with the type I IFN pathway in patients with polymyositis

Louise Ekholm1, J Michelle Kahlenberg2, Sevim Barbasso Helmers3

  • 1Department of Medicine, Rheumatology Unit, Karolinska University Hospital, Karolinska Institutet, Solna, Sweden louise.ekholm@karolinska.se.

Rheumatology (Oxford, England)
|August 8, 2016
PubMed
Abstract

Insights

Polymyositis and dermatomyositis (PM/DM) patients have fewer endothelial progenitor cells (EPCs) with impaired function. Type I interferon and IL-18 pathways contribute to this dysregulation, impacting vascular health.

Area of Science:

  • Immunology
  • Vascular Biology
  • Rheumatology

Background:

  • Endothelial progenitor cell (EPC) dysfunction is linked to poor vascular outcomes.
  • Polymyositis and dermatomyositis (PM/DM) are autoimmune conditions affecting muscles and skin.

Purpose of the Study:

  • To investigate EPC dysregulation in PM/DM patients.
  • To determine the role of type I interferon (IFN) and IL-18 in PM/DM-associated EPC dysfunction.

Main Methods:

  • Flow cytometry quantified circulating EPCs in PM/DM patients and controls.
  • EPC differentiation capacity was assessed with and without PM/DM serum and neutralizing antibodies.
  • Serum type I IFN activity and IL-18 concentrations were measured.

Main Results:

  • PM/DM patients had significantly lower circulating EPCs compared to controls.
  • PM/DM EPCs showed reduced differentiation capacity, inhibited by PM/DM serum.
  • Neutralizing antibodies to IL-18 or type I IFN receptor partially reversed these effects.

Conclusions:

  • PM/DM is associated with impaired EPC phenotype and function.
  • Aberrant IL-18 and type I IFN pathways likely contribute to EPC dysregulation in PM/DM.
  • Further research is needed to determine the clinical implications for vasculopathy.
Keywords:
IFN-regulated gene expressionIL-18autoantibodiesidiopathic inflammatory myopathiesinterferon signature

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