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Influence of stimulatory and suppressive DNA motifs on host susceptibility to inflammatory arthritis

Rainald A Zeuner1, Daniela Verthelyi, Mayda Gursel

  • 1II Medical Clinic, University of Kiel, Kiel, Germany.

Arthritis and Rheumatism
|June 10, 2003
PubMed
Abstract

Insights

Systemic administration of immunostimulatory (CpG) oligodeoxynucleotides (ODNs) increases susceptibility to inflammatory arthritis, while suppressive ODNs decrease it. CD11c+ cells mediate this effect, suggesting therapeutic potential for suppressive ODNs in inflammatory diseases.

Area of Science:

  • Immunology
  • Molecular Biology
  • Rheumatology

Background:

  • Oligodeoxynucleotides (ODNs) are short DNA sequences with immunomodulatory properties.
  • CpG ODNs are known to activate immune responses, while other ODNs can suppress them.
  • Host susceptibility to inflammatory arthritis can be influenced by systemic immune modulation.

Purpose of the Study:

  • To investigate the impact of systemic immunostimulatory and immunosuppressive ODNs on the development of inflammatory arthritis.
  • To determine the role of specific immune cells in mediating arthritis susceptibility following ODN treatment.

Main Methods:

  • BALB/c mice were systemically treated with either CpG ODNs or suppressive ODNs.
  • Mice were subsequently challenged intraarticularly with CpG DNA to induce arthritis.
  • The onset and severity of the inflammatory response were monitored.

Main Results:

  • Systemic CpG ODN treatment significantly enhanced susceptibility to local inflammation and arthritis.
  • Systemic suppressive ODN treatment reduced susceptibility to inflammatory arthritis.
  • CD11c+ cells were identified as critical mediators of host sensitivity, producing TNF-alpha and transferring resistance.

Conclusions:

  • Systemic administration of immunostimulatory and immunosuppressive ODNs significantly influences host susceptibility to local inflammatory challenges like arthritis.
  • Suppresssive ODNs demonstrate potential as a preventative or therapeutic strategy for pro-inflammatory diseases.

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