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Mechanisms of cartilage degradation in inflammatory arthritis: interaction between chondrocytes and immunoglobulin G.
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1993
Year
ImmunologyCartilage DegradationMusculoskeletal ResearchOrthopaedic SurgeryInflammatory ArthritisInflammationRheumatoid DisorderCartilage DegenerationOsteoarthritisInflammatory Rheumatic DiseaseRheumatoid ArthritisImmune ComplexesRheumatologyAutoimmune DiseaseBovine ChondrocytesImmunoglobulin GAutoimmunityInflammatory DiseaseCell BiologyAnti-inflammatoryMedicine
A possible role for immune complexes in the degradation of cartilage (rheumatoid arthritis and antigen induced arthritis) has been modelled in vitro by studying interactions between cultured bovine chondrocytes and monomeric (M) or heat aggregated (HA) IgG. Concentrations of IgG used were within the range of values reported in the synovial fluids of rheumatoid joints. ELISA and rosetting assays revealed Fc receptor mediated binding of MIgG and HAIgG to chondrocytes that had been cultured, but not to freshly isolated cells. Both forms of IgG stimulated the production of metalloprotease, but only HAIgG boosted generation of superoxide anion and reduced proteoglycan synthesis. HAIgG also stimulated cells to produce immunoreactive interleukin 1 although no biological activity was apparent. It is concluded that the equivalent behavior of chondrocytes in vivo, triggered by immune complexes, could contribute or lead directly to matrix degradation.