ArticleThe Journal of clinical investigation2000
Cytotoxic mAb from rheumatic carditis recognizes heart valves and laminin.
Article in The Journal of clinical investigation, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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
97 citing papers in PubMed, 242 citations in OpenAlex.
- Usefulness of immunosuppression for giant cell myocarditis.The American journal of cardiology · 2008Trial
- Heart-specific T cell responses: from antigens to disease mechanisms.Nature reviews. Cardiology · 2026Review
- Inflammatory and hormonal crosstalk linking rheumatic fever to chronic valvular heart disease.Molecular biology reports · 2026Review
- Rheumatic heart disease in children and adolescents, part 1: epidemiology, pathogenesis and diagnosis.BMJ paediatrics open · 2026Review
- Valve biology and rheumatic heart disease pathogenesis.Nature cardiovascular research · 2026Review
- Acute rheumatic fever and rheumatic heart disease.Nature reviews. Disease primers · 2026Review
- Article
- Mechanisms of mitral valve development and disease.Frontiers in cardiovascular medicine · 2026Review
- Revisiting the streptococcal M protein: modern perspectives on antibody function, host interactions, and therapeutic targeting.Frontiers in immunology · 2026Review
- Editor's Choice Platform for identifying human glycan-specific antibodies against bacterial pathogens using synthetic glycan fragments.Glycobiology · 2025Article
- No compelling evidence that vaccination with streptococcus pyogenes group A carbohydrate elicits cross-reactive rheumatic fever autoantibodies.NPJ vaccines · 2025Review
- Inflammatory Responses Potentiate GAS M Protein Induced Cardiac Damage in an Experimental Model of Rheumatic Heart Disease.Immunity, inflammation and disease · 2025Article
- Investigation of Asymptomatic Rhythm and Conduction System Disorders in Pediatric Patients Diagnosed with Acute Rheumatic Fever According to Current Guidelines.Turkish archives of pediatrics · 2025Article
- From Infection to Autoimmunity:Microorganisms · 2025Review
- Cardiac autoantibodies promote a fibrotic transcriptome and reduced ventricular recovery in human myocarditis.Frontiers in immunology · 2025Article
- The roles of immuno-modulator treatment and echocardiographic screening in rheumatic fever and rheumatic heart disease control: research from Aotearoa, New Zealand.Journal of the Royal Society of New Zealand · 2025Review
- Acute rheumatic fever: 15-year single-center experience of a middle-income country in Latin America.Archivos de cardiologia de Mexico · 2025Article
- A mini review of the pathogenesis of acute rheumatic fever and rheumatic heart disease.Frontiers in cellular and infection microbiology · 2025Review
- Review
- Pediatric acute-onset neuropsychiatric syndrome and pediatric autoimmune neuropsychiatric disorder associated with streptococcal infections: a delphi study and consensus document about definition, diagnostic criteria, treatment and follow-up.Frontiers in immunology · 2024Article
37 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Anti-streptococcal antibodies cross-reactive with N-acetyl-betaD-glucosamine (GlcNAc) and myosin are present in the sera of patients with rheumatic fever (RF). However, their role in tissue injury is not clear. In this study, we show that anti-GlcNAc/anti-myosin mAb 3.B6 from a rheumatic carditis patient was cytotoxic for human endothelial cell lines and reacted with human valvular endothelium and underlying basement membrane. Reactivity of mAb 3.B6 with the valve was inhibited by human cardiac myosin > laminin > GlcNAc. The mAb 3.B6 epitopes were localized in fragments of human cardiac myosin, including heavy meromyosin (HMM), the S1 subfragment, and two light meromyosin (LMM) peptides containing amino acid sequences KEALISSLTRGKLTYTQQ (LMM 1) and SERVQLLHSQNTSLINQK (LMM 33). A novel feature of mAb 3.B6 was its reactivity with the extracellular matrix protein laminin, which may explain its reactivity with the valve surface. A laminin A-chain peptide (HTQNT) that includes homology to LMM33 inhibited the reactivity of mAb 3.B6 with human valve. These data support the hypothesis that cross-reactive antibodies in rheumatic carditis cause injury at the endothelium and underlying matrix of the valve.
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What OpenQuestion holds
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.