ArticleJournal of immunology (Baltimore, Md. : 1950)2010
C1q deficiency leads to the defective suppression of IFN-alpha in response to nucleoprotein containing immune complexes.
Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 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
70 citing papers in PubMed, 143 citations in OpenAlex.
- Article
- Complement and inflammasome crosstalk in chronic inflammation.Frontiers in immunology · 2026Review
- Systemic lupus erythematosus: updated insights on the pathogenesis, diagnosis, prevention and therapeutics.Signal transduction and targeted therapy · 2025Review
- Autoimmune diseases and atherosclerotic cardiovascular disease.Nature reviews. Cardiology · 2024Review
- Hematopoietic Stem Cell Transplantation for C1q Deficiency: A Study on Behalf of the EBMT Inborn Errors Working Party.Journal of clinical immunology · 2024Article
- Hereditary C1q Deficiency is Associated with Type 1 Interferon-Pathway Activation and a High Risk of Central Nervous System Inflammation.Journal of clinical immunology · 2024Article
- The complement system and human autoimmune diseases.Journal of autoimmunity · 2023Review
- The type I interferonopathies: 10 years on.Nature reviews. Immunology · 2022Review
- Renal diseases and the role of complement: Linking complement to immune effector pathways and therapeutics.Advances in immunology · 2021Review
- Autoantibodies against complement component C1q in systemic lupus erythematosus.Clinical & translational immunology · 2021Review
- Lung involvement in monogenic interferonopathies.European respiratory review : an official journal of the European Respiratory Society · 2020Article
- Type I Interferonopathies: from a Novel Concept to Targeted Therapeutics.Current rheumatology reports · 2020Review
- Neutrophil FcγRIIA availability is associated with disease activity in systemic lupus erythematosus.Arthritis research & therapy · 2020Article
- SLE: Novel Postulates for Therapeutic Options.Frontiers in immunology · 2020Review
- Inverse correlation between serum complement component C1q levels and whole blood type-1 interferon signature in active tuberculosis and QuantiFERON-positive uveitis: implications for diagnosis.Clinical & translational immunology · 2020Article
- Article
- New Attempts to Define and Clarify Lupus.Current rheumatology reports · 2019Review
- Sources of Pathogenic Nucleic Acids in Systemic Lupus Erythematosus.Frontiers in immunology · 2019Review
- Proinflammatory Differentiation of Macrophages Through Microparticles That Form Immune Complexes Leads to T- and B-Cell Activation in Systemic Autoimmune Diseases.Frontiers in immunology · 2019Article
- Rheumatoid arthritis and systemic lupus erythematosus: Pathophysiological mechanisms related to innate immune system.SAGE open medicine · 2019Review
10 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
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Almost all humans with homozygous deficiency of C1q develop systemic lupus erythematosus (SLE). The precise cellular mechanism(s) by which C1q prevents the development of SLE remains unclear. In this study, we tested the role of C1q in the regulation of IFN-α induced by immune complexes (ICs) in vitro, as well as the consequences of lack of C1q in vivo. Our experiments revealed that C1q preferentially promotes the binding of SLE ICs to monocytes rather than plasmacytoid dendritic cells, but this inhibition was not due to the induction of inhibitory soluble factors. The presence of C1q also altered the trafficking of ICs within monocytes such that ICs persisted in early endosomes. In patients with C1q deficiency, serum and cerebrospinal fluid levels of IFN-α and IFN-γ-inducible protein-10 levels were elevated and strongly correlated with Ro autoantibodies, demonstrating the clinical significance of these observations. These studies therefore associate C1q deficiency with defective regulation of IFN-α and provide a better understanding of the cellular mechanisms by which C1q prevents the development of IC-stimulated autoimmunity.
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.