ReviewJournal of clinical immunology2004
Antiphospholipid syndrome infectious origin.
Review in Journal of clinical immunology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
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
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 144 citations in OpenAlex.
- Rheumatic fever associated with antiphospholipid syndrome: systematic review.Journal of immunology research · 2014Pooled it
- Effect of vitamin DClinics (Sao Paulo, Brazil) · 2024Trial
- IgA Anti-β2-Glycoprotein I Antibodies as Markers of Thrombosis and Severity in COVID-19 Patients.Viruses · 2024Article
- Antiphospholipid Antibodies Associated with Native Arteriovenous Fistula Complications in Hemodialysis Patients: A Comprehensive Review of the Literature.Antibodies (Basel, Switzerland) · 2024Review
- Anticardiolipin and anti-beta 2-glycoprotein I antibodies in patients with unexplained articular manifestations.Journal of clinical laboratory analysis · 2023Article
- Myeloproliferative neoplasms - blurring the lines between cancer and chronic inflammatory disorder.Frontiers in oncology · 2023Review
- Pancreatic Pathological Changes in Murine Toxoplasmosis and Possible Association with Diabetes Mellitus.Biomedicines · 2022Article
- COVID-19 and the antiphospholipid syndrome.Autoimmunity reviews · 2022Review
- Endothelial Cell-Activating Antibodies in COVID-19.Arthritis & rheumatology (Hoboken, N.J.) · 2022Article
- COVID-19 coagulopathy and antiphospholipid syndrome.Revista colombiana de reumatologia · 2022Review
- Antigens and Antibodies of the Antiphospholipid Syndrome as New Allies in the Pathogenesis of COVID-19 Coagulopathy.International journal of molecular sciences · 2022Review
- Circulating immune-complexes of IgG/IgM bound to B2-glycoprotein-I associated with complement consumption and thrombocytopenia in antiphospholipid syndrome.Frontiers in immunology · 2022Observational
- Do common infections trigger disease-onset or -severity in CTLA-4 insufficiency?Frontiers in immunology · 2022Article
- Dorsolateral medullary infarction during skin infection by Stenotrophomonas maltophilia in a patient with triple antiphospholipid antibody positivity: a case-based review.Clinical rheumatology · 2021Review
- Prothrombotic autoantibodies in serum from patients hospitalized with COVID-19.Science translational medicine · 2020Article
- Molecular Mechanisms of "Antiphospholipid Antibodies" and Their Paradoxical Role in the Pathogenesis of "Seronegative APS".International journal of molecular sciences · 2020Review
- Hyperthrombotic Milieu in COVID-19 Patients.Cells · 2020Review
- The IgA Isotype of Anti-β2 Glycoprotein I Antibodies Recognizes Epitopes in Domains 3, 4, and 5 That Are Located in a Lateral Zone of the Molecule (L-Shaped).Frontiers in immunology · 2019Article
- Article
- Pathophysiology of the cochlear intrastrial fluid-blood barrier (review).Hearing research · 2016Review
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Antiphospholipid syndrome (APS) is characterized by the presence of pathogenic autoantibodies against beta 2-glycoprotein-I (beta 2GPI). The factors causing production of anti-beta 2GPI remain unidentified, but an association with infectious agents has been reported. Studies on experimental APS models proved that molecular mimicry between beta 2GPI-related synthetic peptides and structures within bacteria, viruses, tetanus toxoid, and CMV are a cause for experimental APS. Any explanation of how microbial infections might set off APS must take into account the observation that all individuals appear to harbor potentially autoreactive lymphocytes, as well as natural antiphospholipid antibodies, but that these cells or antibodies remain innocuous unless somehow activated. Herein, we discuss the association of antiphospholipid antibodies in the infectious state, molecular mimicry as a proposed cause for development of APS, and the contribution of the database to this topic.
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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.