RHEUMATOID-FACTOR, ANTI-HEAT SHOCK PROTEIN (65 KDA) ANTIBODIES AND ANTINUCLEAR ANTIBODIES IN EQUINE JOINT DISEASES

Citation
Sd. Carter et al., RHEUMATOID-FACTOR, ANTI-HEAT SHOCK PROTEIN (65 KDA) ANTIBODIES AND ANTINUCLEAR ANTIBODIES IN EQUINE JOINT DISEASES, Equine veterinary journal, 27(4), 1995, pp. 288-295
Citations number
61
Categorie Soggetti
Veterinary Sciences
Journal title
ISSN journal
04251644
Volume
27
Issue
4
Year of publication
1995
Pages
288 - 295
Database
ISI
SICI code
0425-1644(1995)27:4<288:RASP(K>2.0.ZU;2-M
Abstract
To consider the hypothesis that autoimmune mechanisms may contribute t o the pathology of equine joint diseases, 3 autoimmune responses were assayed in sera and synovial fluids, IgM-rheumatoid factor and antibod ies to heat shock protein 65 kDa were determined by ELISA; anti-nuclea r antibodies were assayed by indirect immunofluorescence to whole cell nuclear components, Ah parameters showed only modest increases, if an y and not in a pattern related to disease, although some statistically significant increases were detected. Group analysis showedsignificant ly elevated synovial fluid IgM-rheumatoid factor (IgM-RF) in horses wi th OA (P<0.01), traumatised joints (P<0.01) and articular fractured bo nes P<0.001). There was no significantly increased IgM-RF in the sera of horses with joint disorders compared to control horses. Significant ly raised anti-heat shock protein molecular weight 65 kDa (HSP65) anti bodies were only found in the synovial fluids of the horses with traum atised joints (P<0.001). No correlations were found between the synovi al fluid and sera levels of IgM-RF or anti-HSP65 antibodies. Synovial fluid anti-HSP65 antibody and IgM-RF levels positively correlated in t he OCD (P<0.001), fracture (P<0.01) and synovitis (P<0.05) groups, As antibodies to HSP65 correlated with IgG concentrations in synovial flu ids, it is not possible to draw conclusions on HSP-roles in joint dise ase pathogenesis, No serum anti-nuclear antibodies (ANA) were detected by immunofluorescence using rat liver and a human epithelial cell lin e (HEp-2) as substrates. Compared with autoimmune responses in human a nd canine arthropathies, the low levels of autoimmune reactivity detec ted in this study can only suggest a minor contributory role to joint disease pathology in the horse, These results have 2 important implica tions, Firstly, other pathogenetic mechanisms should be considered and secondly autoimmune mechanisms cannot be used to monitor disease prog ress and therefore should not be targetted for treatment.