ArticleThe Journal of clinical investigation2003
Complement system on the attack in autoimmunity.
Article in The Journal of clinical investigation, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 23 citations in OpenAlex.
- The complement system and human autoimmune diseases.Journal of autoimmunity · 2023Review
- Opposite Profiles of Complement in Antiphospholipid Syndrome (APS) and Systemic Lupus Erythematosus (SLE) Among Patients With Antiphospholipid Antibodies (aPL).Frontiers in immunology · 2019Article
- C5a induces caspase-dependent apoptosis in brain vascular endothelial cells in experimental lupus.Immunology · 2016Article
- Blockade of autoantibody-initiated tissue damage by using recombinant fab antibody fragments against pathogenic autoantigen.The American journal of pathology · 2010Article
- Tracing the molecular pathogenesis of antiphospholipid syndrome.The Journal of clinical investigation · 2008Article
- The alternative complement pathway revisited.Journal of cellular and molecular medicine · 2008Review
- The quantitative role of alternative pathway amplification in classical pathway induced terminal complement activation.Clinical and experimental immunology · 2004Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The antiphospholipid syndrome is characterized clinically by fetal loss and thrombosis and serologically by the presence of autoantibodies to lipid-binding proteins. In a model of this procoagulant condition in which these antibodies are injected into pregnant mice, fetal loss was prevented by blocking of complement activation. Specifically, interaction of complement component 5a (C5a) with its receptor is necessary for thrombosis of placental vasculature. Inhibition of complement activation may have a therapeutic role in this disease.
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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.