Anti-M₃ Muscarinic Acetylcholine Receptor Antibodies in Systemic Lupus Erythematosus

Abstract

Background : Evidences have shown that anti-M 3 muscarinic acetylcholine receptor IgG (anti-M 3 mAChR IgG) are clinically useful autoantibody that exert a cholinergic pharmacologic effect binding and interacting with M 3 mAChR at the level of exocrine gland (salivary and ocular). Aims : The aim of this study was to determine the associations between serum level of anti-M 3 mAChR IgG in patients with systemic lupus erythematosus (SLE) and other autoantibodies, serum prostaglandin E 2 (PGE 2 ), and clinical manifestations. Methods : Serum autoantibodies against M 3 mAChR synthetic peptide were measured by enzyme-linked immuno absorbent assay (ELISA) using, as an antigen, a 25-mer peptide K-R-T-V-P-D-N-Q-C-F-I-Q-F-L-S-N-P-A-V-T-F-G-T-A-I corresponding to the amino acid sequence of the second extracellular loop of the human M 3 mAChR. Serum levels of antinuclear antibodies (ANA), anti-Smith (Sm) antibodies, anti-phospholipid (APL) antibodies, and PGE 2 were determined by ELISA in patients with SLE. Results : We found significantly enhanced titers of anti-M 3 mAChR IgG in sera from SLE patients compared with healthy individuals (control). In addition, serum levels of PGE 2 were significantly higher in SLE patients than in control patients and were significantly higher in active than in non-active SLE. No correlation was found with other autoantibodies present in SLE. By contrast, a positive correlation was found between anti-M 3 mAChR IgG and PGE 2 serum levels in SLE. Conclusions : As anti-M 3 mAChR antibodies present in the sera of SLE patients may be another factor in the pathogenesis of this disease, and the increment of PGE 2 in the sera of SLE has a modulatory action on the inflammatory process, suggesting that the presence of these autoantibodies against M 3 mAChR may contribute to sustained immune deregulation and the strong inflammatory component observed in SLE.