Anti-ribosomal P protein antibodies detected by immunoblotting in patientswith connective tissue diseases: their specificity for SLE and associationwith IgG anticardiolipin antibodies
A. Ghirardello et al., Anti-ribosomal P protein antibodies detected by immunoblotting in patientswith connective tissue diseases: their specificity for SLE and associationwith IgG anticardiolipin antibodies, ANN RHEUM D, 59(12), 2000, pp. 975-981
Objective-To assess the prevalence and clinical and serological association
s of anti-ribosomal P protein antibodies (anti-P antibodies) in patients wi
th connective tissue diseases (CTDs) and investigate the immunobiological n
ature of autoantibody clustering in which anti-P antibodies play a part.
Methods-IgG anti-P antibodies in the sera of 267 patients with CTDs and 31
healthy subjects were analysed by immunoblotting performed on cytoplasmic e
xtract of Rail cells. 60 patients with systemic lupus erythematosus (SLE),
32 systemic sclerosis, 46 primary Sjogren's syndrome, 16 poly/dermatomyosit
is, 11 rheumatoid arthritis, 8 undifferentiated CTD, 72 overlap CTD, and 22
primary antiphospholipid syndrome were studied. Anti-P antibodies were aff
inity purified by elution from nitrocellulose bound antigen and tested by E
LISA for their binding activity to cardiolipin.
Results-Anti-P antibodies were detected in 16 (6%) patients and in none of
the controls: 12/60 SLE (20%) and 4/80 undifferentiated/overlap patients wi
th CTD (5%). A close association of IgG antibodies with P proteins and with
cardiolipin was seen in lupus sera (p=0.0009, odds ratio 18.33). Anti-P an
tibodies from 9 of 12 anti-P lupus serum samples could be affinity purified
and none of the affinity purified fractions cross reacted with ELISA plate
coated cardiolipin.
Conclusions-Anti-P immunoreactivity is a specific marker of SLE and lupus-l
ike disease and its detection is recommended as a powerful diagnostic tool.
Anti-P antibodies are strongly clustered with IgG anticardiolipin antibodi
es in lupus sera, even if they are independently elicited. This suggests th
at their cognate autoantigens play a part in a common pathogenetic pathway
in SLE.