ArticleJournal of immunology (Baltimore, Md. : 1950)2009
Type I interferons produced by resident renal cells may promote end-organ disease in autoantibody-mediated glomerulonephritis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
What it found
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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.
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Who cites it
63 citing papers in PubMed, 97 citations in OpenAlex.
- Decoding Lupus Diagnosis, Pathogenesis and Therapy: From Systemic Autoimmunity to Renal Damage.Diagnostics (Basel, Switzerland) · 2026Review
- Article
- The Evolution of Lupus Nephritis Therapy from the 1960s to the Present.Bioengineering (Basel, Switzerland) · 2026Review
- Damaged glomeruli in proliferative pediatric lupus nephritis exhibit a C5a-C5aR1 induced fibrotic transcriptional program.bioRxiv : the preprint server for biology · 2026Article
- Pathogenesis of renal involvement in primary Sjögren's disease: convergence of multifactorial mechanisms on immune dysregulation.Frontiers in immunology · 2026Review
- Type I interferon drives T cell cytotoxicity by upregulation of interferon regulatory factor 7 in autoimmune kidney diseases in mice.Nature communications · 2025Article
- Targeting the Type I Interferon Pathway in Glomerular Kidney Disease: Rationale and Therapeutic Opportunities.Kidney international reports · 2025Review
- Interferon-α as a biomarker to predict renal outcomes in lupus nephritis.Lupus science & medicine · 2024Article
- Expression of myxovirus resistance protein A in lupus nephritis and other glomerular nephropathies.Journal of nephrology · 2024Article
- Type I IFN in Glomerular Disease: Scarring beyond the STING.International journal of molecular sciences · 2024Review
- Transcription Factors in the Pathogenesis of Lupus Nephritis and Their Targeted Therapy.International journal of molecular sciences · 2024Review
- Circulating neutrophil extracellular trap remnants as a biomarker to predict outcomes in lupus nephritis.Lupus science & medicine · 2024Article
- Therapeutically targeting proinflammatory type I interferons in systemic lupus erythematosus: efficacy and insufficiency with a specific focus on lupus nephritis.Frontiers in immunology · 2024Review
- Sirtuin 3 is required for the dexmedetomidine-mediated alleviation of inflammation and oxidative stress in nephritis.Immunity, inflammation and disease · 2024Article
- How Neutrophils Shape the Immune Response: Reassessing Their Multifaceted Role in Health and Disease.International journal of molecular sciences · 2023Review
- Pathogenic cellular and molecular mediators in lupus nephritis.Nature reviews. Nephrology · 2023Review
- Decipher the Immunopathological Mechanisms and Set Up Potential Therapeutic Strategies for Patients with Lupus Nephritis.International journal of molecular sciences · 2023Review
- Urinary markers differentially associate with kidney inflammatory activity and chronicity measures in patients with lupus nephritis.Lupus science & medicine · 2023Article
- Brensocatib, an oral, reversible inhibitor of dipeptidyl peptidase 1, mitigates interferon-α-accelerated lupus nephritis in mice.Frontiers in immunology · 2023Article
- CD11b agonists offer a novel approach for treating lupus nephritis.Translational research : the journal of laboratory and clinical medicine · 2022Review
3 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
11 authors at 3 institutions in 1 country.
Funding
Abstract
Increased Type I IFNs or IFN-I have been associated with human systemic lupus erythematosus. Interestingly augmenting or negating IFN-I activity in murine lupus not only modulates systemic autoimmunity, but also impacts lupus nephritis, suggesting that IFN-I may be acting at the level of the end-organ. We find resident renal cells to be a dominant source of IFN-I in an experimental model of autoantibody-induced nephritis. In this model, augmenting IFN-I amplified antibody-triggered nephritis, whereas ablating IFN-I activity ameliorated disease. One mechanism through which increased IFN-I drives immune-mediated nephritis might be operative through increased recruitment of inflammatory monocytes and neutrophils, though this hypothesis needs further validation. Collectively, these studies indicate that an important contribution of IFN-I toward the disease pathology seen in systemic autoimmunity may be exercised at the level of the end-organ.
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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.