ArticleClinical immunology (Orlando, Fla.)2015
Signal transducer and activator of transcription (STAT) 3 inhibition delays the onset of lupus nephritis in MRL/lpr mice.
Article in Clinical immunology (Orlando, Fla.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 82 citations in OpenAlex.
- Review
- APLNR reduction in kidney-muscle crosstalk in renal model recovered by exercise and STAT3 inhibition.Biochemistry and biophysics reports · 2026Article
- Targeting JAK/STAT signalling with cold atmospheric plasma: a potential therapy for systemic lupus erythematosus.Expert reviews in molecular medicine · 2026Review
- Targeting STAT3 in systemic lupus erythematosus and lupus nephritis: mechanisms, therapeutic advances, and structure-informed perspectives.Frontiers in pharmacology · 2026Review
- Single-Cell Transcriptomics Uncover EEF1A1-Driven Ubiquitination Dysregulation in T Cell Exhaustion and SLE Pathogenesis via STAT1-Mediated Th1/Th2 Imbalance.Mediators of inflammation · 2025Article
- CD3Frontiers in immunology · 2025Review
- STAT3 inhibition ameliorates renal interstitial inflammation in MRL/lpr mice with diffuse proliferative lupus nephritis.Renal failure · 2024Article
- JAK Inhibition as a Potential Treatment Target in Systemic Lupus Erythematosus.Mediterranean journal of rheumatology · 2024Review
- Inhibition of STAT3 alleviates LPS-induced apoptosis and inflammation in renal tubular epithelial cells by transcriptionally down-regulating TASL.European journal of medical research · 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
- Synergistic effects of BTN3A1, SHP2, CD274, and STAT3 gene polymorphisms on the risk of systemic lupus erythematosus: a multifactorial dimensional reduction analysis.Clinical rheumatology · 2024Article
- DUSP2 inhibits the progression of lupus nephritis in mice by regulating the STAT3 pathway.Open life sciences · 2023Article
- Janus kinase inhibitors in systemic lupus erythematosus: implications for tyrosine kinase 2 inhibition.Frontiers in medicine · 2023Review
- Splicing factor deficits render hematopoietic stem and progenitor cells sensitive to STAT3 inhibition.Cell reports · 2022Article
- Norcantharidin ameliorates the development of murine lupus via inhibiting the generation of IL-17 producing cells.Acta pharmacologica Sinica · 2022Article
- The Behaviour of Serum Survivin in Patients With Lupus Nephritis.Biomarker insights · 2022Article
- Review
- Article
- Glycol chitosan-based tacrolimus-loaded nanomicelle therapy ameliorates lupus nephritis.Journal of nanobiotechnology · 2021Article
- Niclosamide suppresses the expansion of follicular helper T cells and alleviates disease severity in two murine models of lupus via STAT3.Journal of translational medicine · 2021Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The transcription factor STAT3 is overexpressed and hyperactivated in T cells from SLE patients. STAT3 plays a central role in T cell differentiation into Th17 and T follicular helper cells, two subsets that orchestrate autoimmune responses in SLE. Moreover, STAT3 is important in chemokine-mediated T cell migration. To better understand its role in SLE, we inhibited STAT3 in lupus-prone mice using the small molecule Stattic. Stattic-treated mice exhibited delayed onset of proteinuria (3 weeks later than controls), and had lower levels of anti-dsDNA antibodies and inflammatory cytokines. Inhibitor treatment reduced lymphadenopathy, resulted in a 3-fold decrease in total T cell number, and a 4-fold decrease in the numbers of T follicular helper cells. In vitro experiments showed that Stattic-treated T cells exhibited decreased proliferation and a decrease in ability to migrate to CXCL12. We propose that STAT3 inhibition represents a therapeutic target in SLE, particularly lupus nephritis.
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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.