Open AccessCirculating antibodies against rat parotid gland M 3 muscarinic receptors in primary Sjögren's syndrome
Author(s) -
Bacman S.,
SterinBorda L.,
JosÉ Camusso J.,
Arana R.,
Hubscher O.,
Borda E.
Publication year - 1996
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1046/j.1365-2249.1996.42748.x
Subject(s) - muscarinic acetylcholine receptor , quinuclidinyl benzilate , carbachol , antibody , receptor , atropine , endocrinology , medicine , acetylcholine receptor , immunology , autoantibody , chemistry
In this study we demonstrate that IgG present in the sera of patients with primary Sjögren's syndrome (PSS) could bind and activate muscarinic acetylcholine receptors (mAChRs) of rat parotid gland. These antibodies were able to inhibit in a non‐competitive manner the binding of 3 H‐quinuclidinyl benzilate (QNB) to mAChRs of purified rat parotid gland membranes. Moreover, IgG from PSS could modify biological effects mediated by mAChR activation; i.e. decrease cAMP, increase phosphoinositide turnover without affecting cGMP. Atropine and 4‐DAMP blocked all of these effects, and carbachol mimicked them, confirming the M 3 subtype mAChRs mediated PSS IgG action. Neither binding nor biological effect were obtained with IgG from sera of normal women. The prevalence of cholinergic antibody was 100% in PSS, and was independent of Ro/SS‐A and La/SS‐B antibodies. It could be concluded that antibody against mAChRs may be another serum factor to be considered in the pathophysiology of the development of PSS.