ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2016
Role of muscarinic-3 receptor antibody in systemic sclerosis: correlation with disease duration and effects of IVIG.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- Rapid improvement of systemic sclerosis-associated intestinal pseudo-obstruction with intravenous immunoglobulin administration.Rheumatology (Oxford, England) · 2023Pooled it
- Gastrointestinal involvement in systemic sclerosis: A spotlight on small bowel involvement, complications and management.Best practice & research. Clinical rheumatology · 2026Review
- Delayed gastric emptying identifies a high-risk clinical subgroup in patients with systemic sclerosis.Rheumatology (Oxford, England) · 2026Article
- Serum CCL18 May Reflect Multiorgan Involvement with Poor Outcome in Systemic Sclerosis.Biomolecules · 2026Article
- Expert recommendations for the management of fecal incontinence in systemic sclerosis: A report from the World Scleroderma Foundation (WSF) Gastrointestinal "Ad hoc committee".Journal of scleroderma and related disorders · 2026Article
- Cellular Players in Gastrointestinal Involvement of Systemic Sclerosis: Insights into Pathogenesis.Cells · 2025Review
- Systemic sclerosis, main culprits and involved signaling pathways.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Anti-muscarinic 3 antibodies associate with a severe clinical phenotype in patients with systemic sclerosis.Rheumatology (Oxford, England) · 2025Article
- Managing gastrointestinal manifestations in systemic sclerosis, a mechanistic approach.Expert review of clinical immunology · 2024Review
- Autoantibodies Targeting G-Protein-Coupled Receptors: Pathogenetic, Clinical and Therapeutic Implications in Systemic Sclerosis.International journal of molecular sciences · 2024Review
- The Collaborative National Quality and Efficacy Registry for Scleroderma: association of medication use on gastrointestinal tract symptoms in early disease and the importance of tobacco cessation.Clinical and experimental rheumatology · 2023Article
- Subcutaneous immunoglobulin therapy for refractory skin thickening in rapidly progressive systemic sclerosis: A case report and literature review.Journal of scleroderma and related disorders · 2023Review
- Particularly severe form of refractory gastrointestinal involvement in systemic sclerosis.BMJ case reports · 2023Article
- Intravenous Immunoglobulins as Immunomodulators in Autoimmune Diseases and Reproductive Medicine.Antibodies (Basel, Switzerland) · 2023Review
- Systemic sclerosis gastrointestinal dysmotility: risk factors, pathophysiology, diagnosis and management.Nature reviews. Rheumatology · 2023Review
- When natural antibodies become pathogenic: autoantibodies targeted against G protein-coupled receptors in the pathogenesis of systemic sclerosis.Frontiers in immunology · 2023Review
- The Microbiome in Systemic Sclerosis: Pathophysiology and Therapeutic Potential.International journal of molecular sciences · 2022Review
- Treatment of Severe Swallowing Dysfunction in Systemic Sclerosis with IVIG: Role of Antimuscarinic Antibodies.Journal of clinical medicine · 2022Article
- Fecal microbiome in systemic sclerosis, in search for the best candidate for microbiota-targeted therapy for small intestinal bacterial overgrowth control.Journal of scleroderma and related disorders · 2022Article
- Autoantibodies as Biomarker and Therapeutic Target in Systemic Sclerosis.Biomedicines · 2022Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Gastrointestinal dysmotility in systemic sclerosis (SSc) is associated with autoantibodies against muscarinic-3 receptor (M3-R). We investigated the temporal course of the site of action of these autoantibodies at the myenteric neurons (MN) vs. the smooth muscle (SM) M3-R in relation to disease duration, and determined the role of intravenous immunoglobulin (IVIG) in reversing these changes. Immunoglobulins purified from SSc patients (SScIgG) were used to assess their differential binding to MN and SM (from rat colon) employing immunohistochemistry (IHC). Effect of SScIgG on neural and direct muscle contraction was determined by cholinergic nerve stimulation and bethanechol-induced SM contraction. Effects of IVIG and its antigen-binding fragment F(ab')2 on SScIgG binding were studied by enzyme-linked immunosorbent assay (ELISA) of rat colonic longitudinal SM myenteric plexus (LSMMP) lysate and to second extracellular loop peptide of M3-R (M3-RL2). SScIgG from all patients demonstrated significantly higher binding to MN than to SM. With progression of SSc duration, binding at MN and SM increased in a linear fashion with a correlation coefficient of 0.696 and 0.726, respectively (P < 0.05). SScIgG-mediated attenuation of neural and direct SM contraction also increased with disease duration. ELISA analysis revealed that IVIG and F(ab')2 significantly reduced SScIgG binding to LSMMP lysate and M3-RL2. Dysmotility in SSc occurs sequentially, beginning with SScIgG-induced blockage of cholinergic neurotransmission (neuropathy), which progresses to inhibition of acetylcholine action at the SM cell (myopathy). IVIG reverses this cholinergic dysfunction at the neural and myogenic receptors by anti-idiotypic neutralization of SScIgG.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.