ArticleNeurology(R) neuroimmunology & neuroinflammation2023
Jo-1 Antibodies From Myositis Induce Complement-Dependent Cytotoxicity and TREM-1 Upregulation in Muscle Endothelial Cells.
Article in Neurology(R) neuroimmunology & neuroinflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- Chimeric antigen receptor T (CAR-T) cell therapy in non-oncological diseases.Signal transduction and targeted therapy · 2026Review
- Emerging therapies in idiopathic inflammatory myopathies.Journal of neuromuscular diseases · 2026Review
- Cardiovascular risk scores, non-invasive vascular measures and myositis damage index reveal increased cardiovascular risk in idiopathic inflammatory myopathies: a case-control study.BMC rheumatology · 2026Article
- Autoantibody internalization in myositis skeletal muscle: Emerging evidence, mechanistic insights, and therapeutic relevance.Autoimmunity reviews · 2026Review
- Distinct phenotypes and prognosis between Jo-1 and non-Jo-1 subtypes in anti-synthetase syndrome: a retrospective cohort study from China.Clinical rheumatology · 2026Article
- Prognostic value of pulmonary vessel-related structures in rapid progression of idiopathic inflammatory myopathy-associated interstitial lung disease: a retrospective study from two centres.BMJ open respiratory research · 2025Article
- Characterization of Muscle Tissue Cell Diversity and Clinical Implications in Idiopathic Inflammatory Myopathy.Journal of cachexia, sarcopenia and muscle · 2025Article
- Gene expression cluster differences and molecular correlation with the STING pathway in orbital MALT lymphoma and orbital IgG4-related eye disease.Discover oncology · 2025Article
- Integration of clinical and serological biomarkers in a nomogram for predicting interstitial lung disease in idiopathic inflammatory myopathies.BMC rheumatology · 2025Article
- Idiopathic Inflammatory Myopathies: Recent Evidence Linking Pathogenesis and Clinical Features.International journal of molecular sciences · 2025Review
- From promise to practice: evaluating the clinical impact of FcRn inhibition in IgG-mediated autoimmune rheumatic diseases.Frontiers in immunology · 2025Review
- Engineered myovascular tissues for studies of endothelial/satellite cell interactions.Acta biomaterialia · 2024Article
- Contribution of Complement, Microangiopathy and Inflammation in Idiopathic Inflammatory Myopathies.Journal of neuromuscular diseases · 2024Review
- [Significance of anti-Jo-1 antibody's clinical stratification in idiopathic inflammatory myopathy and disease spectrum].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
objectivesMuscle microangiopathy due to dysfunction of endothelial cells because of inflammation is a critical hallmark of dermatomyositis (DM); however, its pathomechanism remains unclear. The aim of this study was to evaluate the effect of immunogloblin G (IgG) from patients with idiopathic inflammatory myopathies (IIM) on muscle endothelial cells in vitro.
methodsUsing a high-content imaging system, we analyzed whether IgG purified from sera from patients with IIM (n = 15), disease controls (DCs: n = 7), and healthy controls (HCs: n = 7) can bind to muscle endothelial cells and induce complement-dependent cellular cytotoxicity.
resultsIgGs from Jo-1 antibody myositis could bind to muscle endothelial cells and caused complement-dependent cell cytotoxicity. RNA-seq demonstrated the upregulation of genes associated with tumor necrosis factor (TNF)-α, triggering receptor expressed on myeloid cells-1 (TREM-1), CD25, and mitochondria pathways after exposure to IgG from the Jo-1, signal recognition particle (SRP), and polymyositis (PM) groups. The high-content imaging system showed that TREM-1 expression in the Jo-1, SRP, and PM groups was increased in comparison with DCs and HCs and that the TNF-α expression in the Jo-1 group was higher in comparison with the SRP, PM, DC, and HC groups. The expression of TREM-1 was observed in biopsied capillaries and the muscle membrane from patients with Jo-1 and in biopsied muscle fiber and capillaries from patients with DM and SRP. The depletion of Jo-1 antibodies by IgG of patients with Jo-1 antibody myositis reduced the Jo-1 antibody-induced complement-dependent cellular cytotoxicity in muscle endothelial cells. DISCUSSION: Jo-1 antibodies from Jo-1 antibody myositis show complement-dependent cellular cytotoxicity in muscle endothelial cells. IgGs from patients with Jo-1, SRP, and DM increase the TREM-1 expression in endothelial cells and muscles.
Indexed as
Identifiers
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.