Role of M<sub>3</sub> Muscarinic Acethylcholine Receptor Antibodies as a New Marker in Primary Sjögren Syndrome

Abstract

Aims: This paper investigates the presence of M 3 muscarinic acetylcholine receptor autoantibody present in the serum of patients with primary Sjögren syndrome (pSS). Main methods: We detected the levels of M 3 mAChR peptide IgG, PGE 2 , IL-1β in serum of SS patients using the enzyme-linked immune sorbent assay (ELISA). To measure the quantity of nitrite/nitrate, we used Griess reagent system. Key findings: Titres of M 3 mAChR antibody in sera from SS patients are significantly enhanced compared to healthy subjects (control). The enhancement of these autoantibodies is accompanied by the increase of the levels of PGE 2 , IL-1β and nitrite/nitrate in serum. Under in vitro conditions, the synthetic human M 3 peptide impaires the increment of M 3 mAChR antibody but not that of nati-Ro/SSA antibody. In positive anti-Ro/SSA antibody patients, the increment of M 3 mAChR peptide IgG and the measured pro-inflammatory substances is related. Significance: On this basis, anti M 3 mAChR peptide IgG can be said to act as a modulator of the immune system and to play a role in the host-chronic increment of proinflammatory substances in SS patients with positive Ro/SSA antibody. This association between the antibody and the pathogenesis of SS disease may result in useful predicting SS.

Population-based study suggests an increased risk of Alzheimer’sdisease in Sjögren’s syndrome

“…Their localization is mainly cytoplasmic, and the increased expression of Ro52 in SS and SLE patients is probably implicated positively or negatively in the alteration of cellular immune responses and in the increased apoptosis observed in primary SS patients. Ro52 in primary SS can act as a negative regulator of interferon production, ubiquitination, and degradation of the transcription factors IRF-3, IRF-7, and IRF-8 inducing major alterations in cytokine expression and production [ 24 ]. The inflammatory response is associated with an increased risk of cognitive decline [ 25 ].…”