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CC chemokine receptor (CCR)-2 prevents arthritis development following infection by Mycobacterium avium

Marlon P Quinones1, Fabio Jimenez, Hernan Martinez

  • 1South Texas Veterans Health Care System, Audie L. Murphy Division, San Antonio, Veterans Administration Center for Research on AIDS and HIV-1 Infection, San Antonio, TX, USA.

Journal of Molecular Medicine (Berlin, Germany)
|March 8, 2006
PubMed

Insights

Genetic inactivation of CC chemokine receptor 2 (CCR2) increases arthritis susceptibility in DBA/1j mice. This suggests CCR2 negatively regulates murine arthritis, impacting potential human therapies.

Area of Science:

  • Immunology
  • Rheumatology
  • Genetics

Background:

  • Host factors influencing autoimmune arthritis remain incompletely understood.
  • Previous studies indicated CC chemokine receptor 2 (CCR2) genetic inactivation increases arthritis susceptibility in DBA/1j mice.
  • The role of CCR2 in autoimmune disease pathogenesis requires further elucidation.

Purpose of the Study:

  • To investigate the role of CCR2 in autoimmune arthritis development following infectious and non-infectious challenges.
  • To compare arthritis phenotypes in Ccr2-null mice on different genetic backgrounds (DBA/1j vs. BALB/c).
  • To evaluate the potential of Ccr2-null DBA/1j mice as a model for arthritis research.

Main Methods:

  • Induction of arthritis via collagen type II (CII) and complete Freund's adjuvant (CFA) immunization.
  • Intradermal infection with Mycobacterium avium in Ccr2-null and wild-type mice on DBA/1j and BALB/c backgrounds.
  • Assessment of arthritis phenotype, bacterial burden, interferon gamma (IFNgamma) production, and autoantibody titers.

Main Results:

  • Ccr2-null DBA/1j mice exhibited increased susceptibility to arthritis after both CII/CFA and M. avium challenges.
  • Ccr2-null BALB/c mice failed to develop arthritis despite high bacterial burdens and low IFNgamma production.
  • Ccr2-null DBA/1j mice showed low bacterial burdens, normal IFNgamma, and high anti-CII autoantibody titers.

Conclusions:

  • CCR2 acts as a negative regulator of murine arthritis, with its absence exacerbating disease in a genetically susceptible background.
  • Findings suggest caution in developing CCR2 blockers for human arthritis and related diseases.
  • Ccr2-null DBA/1j mice represent a valuable model for studying arthritis immunopathogenesis and evaluating anti-arthritic agents.

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