Rheumatoid factor, anti‐heat shock protein (65 kDa) antibodies and anti‐nuclear antibodies in equine joint diseases

Summary To consider the hypothesis that autoimmune mechanisms may contribute to the pathology of equine joint diseases, 3 autoimmune responses were assayed in sera and synovial fluids. IgM‐rheumatoid factor and antibodies to heat shock protein 65 kDa were determined by ELISA; anti‐nuclear antibodies were assayed by indirect immunofluorescence to whole cell nuclear components. All parameters showed only modest increases, if any and not in a pattern related to disease, although some statistically significant increases were detected. Group analysis showed significantly elevated synovial fluid IgM‐rheumatoid factor (IgM‐RF) in horses with OA (P<0.01), traumatised joints (P<0.01) and articular fractured bones (P<0.001). There was no significantly increased IgM‐RF in the sera of horses with joint disorders compared to control horses. Significantly raised anti‐heat shock protein molecular weight 65 kDa (HSP65) antibodies were only found in the synovial fluids of the horses with traumatised joints (P<0.001). No correlations were found between the synovial fluid and sera levels of IgM‐RF or anti‐HSP65 antibodies. Synovial fluid anti‐HSP65 antibody and IgM‐RF levels positively correlated in the OCD (P<0.001), fracture (P<0.01) and synovitis (P<0.05) groups. As antibodies to HSP65 correlated with IgG concentrations in synovial fluids, it is not possible to draw conclusions on HSP roles in joint disease pathogenesis. No serum anti‐nuclear antibodies (ANA) were detected by immunofluorescence using rat liver and a human epithelial cell line (HEp‐2) as substrates. Compared with autoimmune responses in human and canine arthropathies, the low levels of autoimmune reactivity detected in this study can only suggest a minor contributory role to joint disease pathology in the horse. These results have 2 important implications. Firstly, other pathogenetic mechanisms should be considered and secondly, autoimmune mechanisms cannot be used to monitor disease progress and therefore should not be targetted for treatment.