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Immunity to cartilage proteoglycans.

S Banerjee1, A R Poole

  • 1Joint Diseases Laboratory, Shriners Hospital for Crippled Children, Montreal, PQ, Canada.

The Journal of Rheumatology. Supplement
|April 1, 1992
PubMed
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Autoimmune responses to cartilage proteoglycans can cause arthritis. Molecular mimicry with bacterial proteins may trigger these pathogenic autoimmune reactions, contributing to rheumatic diseases.

Area of Science:

  • Immunology
  • Rheumatology
  • Biochemistry

Background:

  • Cartilage proteoglycans are key components of articular cartilage.
  • Immune responses to cartilage proteoglycans are implicated in human rheumatic diseases.
  • Animal models suggest a pathological role for autoimmune reactions to proteoglycans.

Purpose of the Study:

  • To investigate the potential for autoimmune responses to cartilage proteoglycans to induce arthritis.
  • To explore the role of molecular mimicry in eliciting pathogenic autoimmune reactions to cartilage proteoglycans.

Main Methods:

  • Immunization of BALB/c mice with human cartilage proteoglycan in adjuvant.
  • Assessment of induced arthritis (peripheral and spondylitis).
  • Evaluation of immune reactivity to mouse cartilage proteoglycan.

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Main Results:

  • Immunization induced peripheral arthritis and spondylitis in mice.
  • Immune reactivity to mouse cartilage proteoglycan was observed.
  • Molecular mimicry with bacterial heat shock proteins may elicit pathogenic autoimmune reactions.

Conclusions:

  • Autoimmune responses to cartilage proteoglycans can induce arthritis in a susceptible host.
  • Bacterial heat shock proteins may act as triggers for autoimmune cartilage damage via molecular mimicry.