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
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.