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- Title
Ganglionic acetylcholine receptor autoantibodies in patients with autoimmune diseases including primary biliary cirrhosis.
- Authors
Yasuhiro Maeda; Shunya Nakane; Osamu Higuchi; Hideki Nakamura; Atsumasa Komori; Kiyoshi Migita; Akihiro Mukaino; Masataka Umeda; Kunihiro Ichinose; Mami Tamai; Shin-ya Kawashiri; Waka Sakai; Hiroshi Yatsuhashi; Atsushi Kawakami; Hidenori Matsuo
- Abstract
Objectives: Autonomic dysfunction is closely associated with autoimmune diseases (AID) including primary biliary cirrhosis (PBC). The objective of this study was to determine the prevalence of anti-ganglionic (nicotinic) acetylcholine receptor (gAChR) antibodies in patients with AID. Methods: We determined the presence of gAChR antibodies in serum samples from 146 patients (systemic lupus erythematosus [SLE]=32; rheumatoid arthritis [RA]=43; systemic sclerosis [SSc]=38; PBC=33) without information regarding autonomic symptoms, as well as 34 patients with other neurological diseases (OND), and 73 healthy controls (HC). We specifically analyzed sera for anti-gAChRa3 and -b4 antibodies using the luciferase immunoprecipitation system (LIPS) assay. Results: LIPS assay detected anti-gAChRa3 and -b4 antibodies in the sera from patients with SLE (12.5%, 4/32), RA (18.6%, 8/43), SSc (13.2%, 5/38), PBC (9.1%, 3/33), OND (2.9%, 1/34), and HC (0.0%, 0/73). There were no significant correlations between the levels of anti-gAChRa3 and -b4 antibodies, and the total titers of autoantibodies in AID. Conclusions: The results demonstrated a significant prevalence of anti-gAChR antibodies in patients with AID, which is independent of the production of other autoantibodies in patients with autoimmune diseases. These anti-gAChR antibodies could mediate the autonomic dysfunction involved in the autoimmune mechanisms of AID.
- Subjects
CHOLINERGIC receptors; AUTOANTIBODIES; AUTOIMMUNE diseases; BILIARY liver cirrhosis; SYSTEMIC lupus erythematosus
- Publication
Modern Rheumatology, 2017, Vol 27, Issue 4, p664
- ISSN
1439-7595
- Publication type
Article
- DOI
10.1080/14397595.2016.1226469