ArticleNature communications2022
Multicellular immune dynamics implicate PIM1 as a potential therapeutic target for uveitis.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 53 citations in OpenAlex.
- Super-enhancer-driven SGK1 activates polyamine metabolism to promote autoimmune uveitis.Science advances · 2026Article
- Immunometabolic regulation and tissue-resident immunity in autoimmune uveitis: from genetic susceptibility to the gut-spleen-eye axis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Protein lactylation in health and diseases: molecular mechanisms, biological significance, and clinical implications.Signal transduction and targeted therapy · 2026Review
- Research Progress on the Regulatory Role of Treg Cells in Inflammatory Eye Diseases.Current issues in molecular biology · 2026Review
- Integrin β3 Promotes Retinal Neovascularization via Endoplasmic Reticulum Stress-Mediated Endothelial Cell Senescence.Investigative ophthalmology & visual science · 2026Article
- PIM1 Inhibition Alleviates Aspergillus fumigatus Keratitis by Regulating DDX41-Mediated STING Signaling Pathway.Investigative ophthalmology & visual science · 2026Article
- Neutrophil membrane-coated and MMP2-responsive nanoparticles deliver PIM1 inhibitor to alleviate inflammatory arthritis through inhibiting Th17 cell differentiation.Journal of nanobiotechnology · 2026Article
- Altered B cell activation contributes to the immunopathogenesis of childhood arthritis-associated uveitis.Nature communications · 2026Article
- Pim1 Serves as a Therapeutic Target for Inflammatory Arthritis via Mitochondrial Metabolism and Th17 Cell Differentiation.Research (Washington, D.C.) · 2026Article
- Metabolic checkpoints in the regulation of Th17 cells: implications for uveitis pathogenesis and therapy.Frontiers in immunology · 2026Review
- Abnormal Elevation of the Expression of Costimulatory Molecule CD226 in Graves' DiseaseEndocrine, metabolic & immune disorders drug targets · 2026Article
- Regulatory T cell dysfunction and exhaustion in uveitis: immunometabolic mechanisms, microenvironmental drivers, and emerging therapeutic strategies.Frontiers in immunology · 2026Review
- Dual role of icaritin in attenuating allograft rejection and exerting antitumor effects in mice.Frontiers in immunology · 2026Article
- Single-cell transcriptomic profiling reveals aberrant CD4⁺ naive T cell differentiation driving immune activation in Behçet's uveitis.Journal of translational medicine · 2025Article
- Effect of Dipyridamole on Experimental Autoimmune Uveitis: Reprogrammed Immune Cell Landscape and Reduced Th17 Pathogenicity.Investigative ophthalmology & visual science · 2025Article
- Inhibition of bruton's tyrosine kinase directly alleviates pathogenic CD4+ T cell response via PPAR-γ signaling in autoimmune uveitis.Journal of neuroinflammation · 2025Article
- Integrated Transcriptome and Metabolomics Analyses Show MYC as a Potential Therapeutic Target for Behçet's Uveitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Histone deacetylases facilitate Th17-cell differentiation and pathogenicity in autoimmune uveitis via CDK6/ID2 axis.Journal of advanced research · 2025Article
- Article
- NETs-CD44-IL-17A Feedback Loop Drives Th17-Mediated Inflammation in Behçet's Uveitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
16 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Uveitis is a severe autoimmune disease, and a common cause of blindness; however, its individual cellular dynamics and pathogenic mechanism remain poorly understood. Herein, by performing single-cell RNA sequencing (scRNA-seq) on experimental autoimmune uveitis (EAU), we identify disease-associated alterations in cell composition and transcriptional regulation as the disease progressed, as well as a disease-related molecule, PIM1. Inhibiting PIM1 reduces the Th17 cell proportion and increases the Treg cell proportion, likely due to regulation of PIM1 to the protein kinase B (AKT)/Forkhead box O1 (FOXO1) pathway. Moreover, inhibiting PIM1 reduces Th17 cell pathogenicity and reduces plasma cell differentiation. Importantly, the upregulation of PIM1 in CD4
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