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, Ah parameters showed only modest increases, if any and not in a pattern related to disease, although some statistically significant increases were detected. Group analysis showedsignificantly 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.