ArticleClinical immunology (Orlando, Fla.)2020
The binding of SLE autoantibodies to mitochondria.
Article in Clinical immunology (Orlando, Fla.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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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
15 citing papers in PubMed, 26 citations in OpenAlex.
- Molecular Mechanisms of Negative Effect of Systemic Lupus Erythematosus on Oogenesis and Meiotic Processes in Oocytes.International journal of molecular sciences · 2026Review
- Antimitochondrial antibodies in systemic lupus erythematosus are associated with and predict nephritis, arterial vascular events, and mortality.Annals of the rheumatic diseases · 2026Article
- MSC-derived exosomes ameliorate systemic lupus erythematosus by reprogramming macrophage mitochondrial homeostasis via the CMPK2-cGAS-STING axis.Journal of nanobiotechnology · 2026Article
- Mitochondrial DNA in systemic lupus erythematosus: pathogenic mechanisms, clinical biomarkers, and precision therapeutic strategies.Frontiers in immunology · 2026Review
- Anti-mitochondrial antibodies as markers of disease activity in childhood-onset systemic lupus erythematosus: a longitudinal cohort study.Rheumatology (Oxford, England) · 2025Article
- Correspondence to editorial on "Prediction of primary biliary cholangitis among health check-up population with anti-mitochondrial M2 antibody positive".Clinical and molecular hepatology · 2025Article
- Unique Interplay Between Antinuclear Antibodies and Nuclear Molecules in the Pathogenesis of Systemic Lupus Erythematosus.Arthritis & rheumatology (Hoboken, N.J.) · 2024Review
- Moonlighting chromatin: when DNA escapes nuclear control.Cell death and differentiation · 2023Review
- The role of mitochondria in rheumatic diseases.Nature reviews. Rheumatology · 2022Review
- Mitochondrial impairment and repair in the pathogenesis of systemic lupus erythematosus.Frontiers in immunology · 2022Review
- Mitochondrial protein CMPK2 regulates IFN alpha-enhanced foam cell formation, potentially contributing to premature atherosclerosis in SLE.Arthritis research & therapy · 2021Article
- Immunometabolic Pathways and Its Therapeutic Implication in Autoimmune Diseases.Clinical reviews in allergy & immunology · 2021Review
- The Role of Immunometabolism in the Pathogenesis of Systemic Lupus Erythematosus.Frontiers in immunology · 2021Review
- Immunometabolism in the pathogenesis of systemic lupus erythematosus: an update.Current opinion in rheumatology · 2020Review
- DNA-nanoparticle interactions: Formation of a DNA corona and its effects on a protein corona.Biointerphases · 2020Article
Corrections and comments
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Authors and funding
6 authors at 5 institutions in 3 countries.
Funding
Abstract
Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterized by immune complexes. Because these complexes contain mitochondrial components, we assessed the presence of antibodies to whole mitochondria (wMITO) using an ELISA in which mitochondria from mouse liver are bound to microtiter plates pre-coated with poly-l-lysine. Studies with this ELISA demonstrated that SLE plasmas contain abundant anti-wMITO activity. While digestion with DNase 1 did not affect anti-wMITO activity, adsorption of plasma on DNA affinity columns could reduce binding activity. Assay for anti-mitochondrial antibodies (AMA) by immunofluorescence and an ELISA with the M2 antigen (2-oxo-acid dehydrogenase protein complex) showed a low frequency of positivity, indicating that AMA and anti-wMITO are distinct specificities. In the study of 204 patients with SLE, the levels of anti-wMITO were higher in active SLE and correlated with levels of anti-DNA. These findings suggest that anti-wMITO can form immune complexes with mitochondria which may drive pathogenesis.
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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.