ArticleFrontiers in immunology2017
The HMGB1-CXCL12 Complex Promotes Inflammatory Cell Infiltration in Uveitogenic T Cell-Induced Chronic Experimental Autoimmune Uveitis.
Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- HMGB1: an overview of its versatile roles in the pathogenesis of colorectal cancer.Cellular oncology (Dordrecht, Netherlands) · 2020Pooled it
- CXCR4 inhibition alleviates prostatic inflammation and pelvic pain via suppressing Th17 cell differentiation and oxidative stress in EAP mice.International journal of biological sciences · 2026Article
- Single-cell transcriptomic profiling reveals aberrant CD4⁺ naive T cell differentiation driving immune activation in Behçet's uveitis.Journal of translational medicine · 2025Article
- Investigation of high-mobility group box 1 variants with lymph node status and colorectal cancer risk.World journal of gastrointestinal oncology · 2025Article
- Single-cell transcriptomic analysis of retinal immune regulation and blood-retinal barrier function during experimental autoimmune uveitis.Scientific reports · 2024Article
- Trimebutine prevents corneal inflammation in a rat alkali burn model.Scientific reports · 2024Article
- RAGE plays key role in diabetic retinopathy: a review.Biomedical engineering online · 2023Review
- Sleep loss potentiates Th17-cell pathogenicity and promotes autoimmune uveitis.Clinical and translational medicine · 2023Article
- The chemokine landscape: one system multiple shades.Frontiers in immunology · 2023Review
- Damage-associated Molecular Patterns in Clinical and Animal Models of Uveitis.Ocular immunology and inflammation · 2022Article
- Damage-Associated Molecular Patterns (DAMPs) in Retinal Disorders.International journal of molecular sciences · 2022Review
- Targeting HMGB1-NFκb Axis and miR-21 by Glycyrrhizin: Role in Amelioration of Corneal Injury in a Mouse Model of Alkali Burn.Frontiers in pharmacology · 2022Article
- Short chain fatty acids inhibit endotoxin-induced uveitis and inflammatory responses of retinal astrocytes.Experimental eye research · 2021Article
- HMGB1 as a therapeutic target in disease.Journal of cellular physiology · 2021Review
- Inhibiting TLR7 Expression in the Retinal Pigment Epithelium Suppresses Experimental Autoimmune Uveitis.Frontiers in immunology · 2021Article
- High Mobility Group Box 1 in Human Cancer.Cells · 2020Review
- The Role of HMGB1, a Nuclear Damage-Associated Molecular Pattern Molecule, in the Pathogenesis of Lung Diseases.Antioxidants & redox signaling · 2019Review
- Suppression of HMGB1 Released in the Glioblastoma Tumor Microenvironment Reduces Tumoral Edema.Molecular therapy oncolytics · 2019Article
- Local S100A8 Levels Correlate With Recurrence of Experimental Autoimmune Uveitis and Promote Pathogenic T Cell Activity.Investigative ophthalmology & visual science · 2018Article
- HMBG1 as a Driver of Inflammatory and Immune Processes in the Pathogenesis of Ocular Diseases.Journal of ophthalmology · 2018Review
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
It is largely unknown how invading autoreactive T cells initiate the pathogenic process inside the diseased organ in organ-specific autoimmune diseases. In experimental autoimmune uveitis (EAU) induced by uveitogenic, interphotoreceptor retinoid-binding protein (IRBP)-specific T cells (tEAU) in mice, we have previously reported that high mobility group box 1 (HMGB1) released as a consequence of the direct interaction between IRBP-specific T cells and retinal parenchymal cells is an early and critical mediator in induction of intraocular inflammation. Our present study explored the roles of HMGB1 in intraocular inflammation, focusing on its role in recruiting inflammatory cells into the eye. Our results showed that supernatants from retinal explants either stimulated with HMGB1 or cocultured with IRBP-specific T cells attracted leukocytes. Notably, HMGB1 antagonists blocked supernatant-induced chemoattraction when present from the start of coculture, but not when added to the culture supernatants after coculture, indicating that molecules released by HMGB1-treated retinal cells are chemoattractive. Moreover, CXCL12 levels in the coculture supernatants were dependent on HMGB1, since they were increased in the cocultures and reduced when HMGB1 antagonists were added at the beginning of the coculture. When either anti-CXCL12 Ab was added to the supernatants after coculture or the responding lymphocytes were pretreated with Ab against CXCL12 specific receptor, CXCR4, chemoattraction by the coculture supernatants was decreased. Finally, induction of tEAU was significantly inhibited by a CXCR4 antagonist, AMD3100, at the time of autoreactive T cell transfer. Our study demonstrates that, at a very early stage of intraocular inflammation initiated by uveitogenic autoreactive T cells, synergism between HMGB1 and CXCL12 is crucial for the infiltration of inflammatory cells.
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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 Socratic graph.