ArticleJournal of immunology (Baltimore, Md. : 1950)2014
TSG-6 inhibits neutrophil migration via direct interaction with the chemokine CXCL8.
Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 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.
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Who cites it
114 citing papers in PubMed, 183 citations in OpenAlex.
- Abnormally low expression of tumor necrosis factor stimulated gene 6 (TSG-6) in obese type 2 diabetic mice contributes to altered inflammation and delayed cutaneous wound healing.bioRxiv : the preprint server for biology · 2026Article
- A diagnostic signatures for intervertebral disc degeneration using TNFAIP6 and COL6A2 based on single-cell RNA-seq and bulk RNA-seq analyses.Annals of medicine · 2025Article
- Investigation of the Impact of Tryptophan-Metabolizing Enzymes and Kynurenic Acid on Antibody-Mediated Glomerulonephritis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- A specific role for endothelial EPLIN-isoform-regulated actin dynamics in neutrophil transmigration.Scientific reports · 2025Article
- Potential drug targets for ovarian cancer identified through Mendelian randomization and colocalization analysis.Journal of ovarian research · 2025Article
- Proteomic profiling of iPSC and tissue-derived MSC secretomes reveal a global signature of inflammatory licensing.NPJ Regenerative medicine · 2025Article
- Effects of Release of TSG-6 from Heparin Hydrogels on Supraspinatus Muscle Regeneration.Tissue engineering. Part A · 2025Article
- TSG-6 promotes healing of critical-sized bone defects in mice.Frontiers in immunology · 2025Article
- TGF-β expressed by M2 macrophages promotes wound healing by inhibiting TSG-6 expression by mesenchymal stem cells.PloS one · 2025Article
- Loss in Pluripotency Markers in Mesenchymal Stem Cells upon Infection withJournal of microbiology and biotechnology · 2024Article
- The roles of hyaluronan in kidney development, physiology and disease.Nature reviews. Nephrology · 2024Review
- The Role of Extracellular Vesicles in Bone Regeneration and Associated Bone Diseases.Current issues in molecular biology · 2024Review
- Biomimetic Hyaluronan Binding Biomaterials to Capture the Complex Regulation of Hyaluronan in Tissue Development and Function.Biomimetics (Basel, Switzerland) · 2024Review
- TSG-6 Is Involved in Fibrous Structural Remodeling after the Injection of Adipose-derived Stem Cells.Plastic and reconstructive surgery. Global open · 2024Article
- TGF-β1 induces formation of TSG-6-enriched extracellular vesicles in fibroblasts which can prevent myofibroblast transformation by modulating Erk1/2 phosphorylation.Scientific reports · 2024Article
- Review
- Endogenous TSG-6 modulates corneal inflammation following chemical injury.The ocular surface · 2024Article
- Mini review: human clinical studies of stem cell therapy in keratoconus.BMC ophthalmology · 2024Review
- A cohort-based study of host gene expression: tumor suppressor and innate immune/inflammatory pathways associated with the HIV reservoir size.PLoS pathogens · 2023Article
- Therapeutic inhibition of CXCR1/2: where do we stand?Internal and emergency medicine · 2023Review
54 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
TNF-stimulated gene/protein-6 (TSG-6) is expressed by many different cell types in response to proinflammatory cytokines and plays an important role in the protection of tissues from the damaging consequences of acute inflammation. Recently, TSG-6 was identified as being largely responsible for the beneficial effects of multipotent mesenchymal stem cells, for example in the treatment of animal models of myocardial infarction and corneal injury/allogenic transplant. The protective effect of TSG-6 is due in part to its inhibition of neutrophil migration, but the mechanisms underlying this activity remain unknown. In this study, we have shown that TSG-6 inhibits chemokine-stimulated transendothelial migration of neutrophils via a direct interaction (KD, ∼ 25 nM) between TSG-6 and the glycosaminoglycan binding site of CXCL8, which antagonizes the association of CXCL8 with heparin. Furthermore, we found that TSG-6 impairs the binding of CXCL8 to cell surface glycosaminoglycans and the transport of CXCL8 across an endothelial cell monolayer. In vivo this could limit the formation of haptotactic gradients on endothelial heparan sulfate proteoglycans and, hence, integrin-mediated tight adhesion and migration. We further observed that TSG-6 suppresses CXCL8-mediated chemotaxis of neutrophils; this lower potency effect might be important at sites where there is high local expression of TSG-6. Thus, we have identified TSG-6 as a CXCL8-binding protein, making it, to our knowledge, the first soluble mammalian chemokine-binding protein to be described to date. We have also revealed a potential mechanism whereby TSG-6 mediates its anti-inflammatory and protective effects. This could inform the development of new treatments for inflammation in the context of disease or following transplantation.
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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.