Journal Article
Research Support, U.S. Gov't, Non-P.H.S.
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The role of muscarinic acetylcholine receptor type 3 polypeptide (M3RP205-220) antibody in the saliva of patients with primary Sjögren's syndrome.

BACKGROUND: Sjögren's syndrome (SS) is a chronic autoimmune disorder of unknown cause. Recent studies have shown that antimuscarinic acetylcholine type 3 receptor (M3R) antibodies can be detected in patients with Sjögren's syndrome (SS), but little is known about the diagnostic value of this antibody.

OBJECTIVES: To assess the clinical correlations of anti-M3R (muscarinic acetylcholine receptor type 3) polypeptide (M3RP205-220) antibodies in saliva from patients of primary Sjögren's syndrome (pSS).

METHODS: Serum samples and unstimulated mixed saliva from 100 patients with SS were collected and examined. Their mean (SD) age was 54.2 (13.4) years, and the mean (SD) disease duration was 6.2 (3.8) years. Serum samples from 40 patients with systemic lupus erythematosus (SLE), 40 with rheumatoid arthritis (RA), and 60 healthy subjects were analysed as controls. All the patients with SS were carefully evaluated according to European and American criteria. A circular M3RP205-220 peptide sequence was synthesized using solid-phase techniques on an applied biosytems peptide synthesizer. The correlation between anti-M3RP205-220 antibodies and clinical manifestations of pSS was analysed.

RESULTS: The IgG of anti-M3RP205-220 antibodies was present in 69% of patients with pSS, 27.5% with SLE, 22.5% with RA, and 23.3% of normal saliva donors. The prevalence of anti-M3RP205-220 antibodies in pSS was significantly higher than in SLE, RA, and normal controls. The specificity of anti-M3RP205-220 antibodies in pSS was 75%. The salivary flow rate in the group positive for anti-M3RP205-220 was 436 μl/10 min, compared to a rate of 658 μl/10 min for the negative group (p<0.05).

CONCLUSIONS: The anti-M3RP205-220 antibody was detected in most patients with pSS. The presence of the antibody was closely associated with the salivary flow rate. This indicated that it may act as an autoantigen, with a role in the pathogenesis of pSS.

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