ArticleNature communications2021
Genetic and chemical inhibition of IRF5 suppresses pre-existing mouse lupus-like disease.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.
- Integration of GWAS and single-cell analysis for psoriasis identifies disease-associated cell subtypes and therapeutic targets.Nature communications · 2026Pooled it
- The role of IRF5 as an immune regulator.Biochemical Society transactions · 2026Review
- The SLC15A4-TASL complex is essential for lupus development in mice.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Leveraging cell-type specificity and similarity improves single-cell eQTL fine-mapping.Nature communications · 2026Article
- scTWAS: a powerful statistical framework for single-cell transcriptome-wide association studies.Nature communications · 2026Article
- Article
- Identifying a Common Autoimmune Gene Core as a Tool for Verifying Biological Significance and Applicability of Polygenic Risk Scores.International journal of molecular sciences · 2026Article
- Glucose metabolic reprogramming in systemic lupus erythematosus and lupus nephritis: theoretical foundations and therapeutic implications.Frontiers in immunology · 2026Review
- The microbiota-systemic lupus erythematosus axis: mechanisms, diagnostics, and therapeutic frontiers.Frontiers in immunology · 2026Review
- Article
- Lyn restrains lupus via kinase-independent mechanisms that limit Toll-like receptor activation and type I interferon responsiveness.Science advances · 2025Article
- scTWAS: A powerful statistical framework for single-cell transcriptome-wide association studies.Research square · 2025Article
- TLR-induced STK25 activation promotes IRF5-mediated inflammation.Life science alliance · 2025Article
- IRF7 controls spontaneous autoimmune germinal center and plasma cell checkpoints.The Journal of experimental medicine · 2025Article
- Immunometabolism in systemic lupus erythematosus.Nature reviews. Rheumatology · 2025Review
- Type 1 interferon signature and allograft inflammatory factor-1 contribute to refractoriness to TNF inhibition in ankylosing spondylitis.Nature communications · 2025Article
- IMPC impact on preclinical mouse models.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Article
- Uncovering latent biological function associations through gene set embeddings.BMC bioinformatics · 2025Article
- Interferon regulatory factor 5 suppresses epithelial-to-mesenchymal transition and metastasis by inducing GATA2 expression in colorectal cancer.Clinical and translational medicine · 2025Article
- Age-Associated B Cells in Autoimmune Diseases: Pathogenesis and Clinical Implications.Clinical reviews in allergy & immunology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor IRF5 has been implicated as a therapeutic target for the autoimmune disease systemic lupus erythematosus (SLE). However, IRF5 activation status during the disease course and the effects of IRF5 inhibition after disease onset are unclear. Here, we show that SLE patients in both the active and remission phase have aberrant activation of IRF5 and interferon-stimulated genes. Partial inhibition of IRF5 is superior to full inhibition of type I interferon signaling in suppressing disease in a mouse model of SLE, possibly due to the function of IRF5 in oxidative phosphorylation. We further demonstrate that inhibition of IRF5 via conditional Irf5 deletion and a newly developed small-molecule inhibitor of IRF5 after disease onset suppresses disease progression and is effective for maintenance of remission in mice. These results suggest that IRF5 inhibition might overcome the limitations of current SLE therapies, thus promoting drug discovery research on IRF5 inhibitors.
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.