ArticleClinical and experimental immunology2018
Tim-3 exacerbates kidney ischaemia/reperfusion injury through the TLR-4/NF-κB signalling pathway and an NLR-C4 inflammasome activation.
Article in Clinical and experimental immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- An Emerging Role of TIM3 Expression on T Cells in Chronic Kidney Inflammation.Frontiers in immunology · 2021Pooled it
- Silencing of HAVCR2 Attenuates Skeletal Muscle Ischemia-Reperfusion Injury by Inhibiting Oxidative Stress.Biochemical genetics · 2026Article
- Serine protease inhibitor from Trichinella spiralis ameliorates diet-induced obesity and adipose tissue inflammation through TIM-3-dependent macrophage reprogramming.PLoS pathogens · 2026Article
- Unlocking the roles of plasma soluble T-cell immunoglobulin and mucin domain-containing protein 3 in kidney diseases: findings from native and allograft biopsy cohorts.Molecular biomedicine · 2026Article
- Tim-3 Deficiency Ameliorates Motor Deficits and Neuroinflammation in MPP+/MPTP-Induced Parkinson's Disease Models via the NF-κB/NLRP3 Pathway.Molecular neurobiology · 2025Article
- Involvement of Tim-3 in Maternal-fetal Tolerance: A Review of Current Understanding.International journal of biological sciences · 2025Review
- Blocking of Tim-3 Ameliorates Spinal Cord Ischemia-Reperfusion Injury Through Inhibiting Neuroinflammation and Promoting M1-to-M2 Phenotypic Polarization of Microglia.Immunity, inflammation and disease · 2024Article
- Human pulmonary microvascular endothelial cells respond to DAMPs from injured renal tubular cells.Pulmonary circulation · 2024Article
- The role of inflammasomes in human diseases and their potential as therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Lipotoxicity and immunometabolism in ischemic acute kidney injury: current perspectives and future directions.Frontiers in pharmacology · 2024Review
- Tim-3 protects against cisplatin nephrotoxicity by inhibiting NF-κB-mediated inflammation.Cell death discovery · 2023Article
- Inflammasome pathway in kidney transplantation.Frontiers in medicine · 2023Review
- Novel insights into NOD-like receptors in renal diseases.Acta pharmacologica Sinica · 2022Review
- Clinical value of the sTim‑3 level in chronic kidney disease.Experimental and therapeutic medicine · 2022Article
- Association of Tim-3/Gal-9 Axis with NLRC4 Inflammasome in Glioma Malignancy: Tim-3/Gal-9 Induce the NLRC4 Inflammasome.International journal of molecular sciences · 2022Article
- T cell immunoglobulin and mucin domain-containing protein 3 is highly expressed in patients with acute decompensated heart failure and predicts mid-term prognosis.Frontiers in cardiovascular medicine · 2022Article
- Evaluation of Inflammasome Activation in Peripheral Blood Mononuclear Cells of Hemodialysis Treated Patients with Glomerulonephritis.Iranian journal of pharmaceutical research : IJPR · 2021Article
- GSK-3β Inhibitor Induces Expression of the TLR4/MyD88/NF-κB Signaling Pathway to Protect Against Renal Ischemia-Reperfusion Injury During Rat Kidney Transplantation.Inflammation · 2019Article
- Tim-3 aggravates podocyte injury in diabetic nephropathy by promoting macrophage activation via the NF-κB/TNF-α pathway.Molecular metabolism · 2019Article
- Labile Heme Aggravates Renal Inflammation and Complement Activation After Ischemia Reperfusion Injury.Frontiers in immunology · 2019Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T cell immunoglobulin domain and mucin domain-containing molecule-3 (Tim-3), a member of the immunoglobulin superfamily, has been shown to play a crucial role in host adaptive immunity and tolerance. However, its role in kidney ischaemia-reperfusion injury (IRI) remains unknown. In this study, we investigated the role and mechanism of Tim-3 signalling after kidney IRI. In an established murine model of kidney IRI, we found that Tim-3 expression is enhanced on monocytes/macrophages. Anti-Tim-3 antibody RMT3-23 ameliorates biochemical and histological kidney injury, reduces apoptosis and decreases macrophage infiltration and cytokine production in ischaemic kidneys. Cell culture experiments also demonstrated that the role of Tim-3 in IRI-induced macrophage activation leads to the secretion of proinflammatory cytokines and chemokines. In addition, Toll-like receptor (TLR)-4 and Nod-like receptor (NLR) family CARD domain-containing protein 4 (NLR-C4) expression were enhanced after kidney IRI and decreased significantly by RMT3-23. Tim-3 not only promotes TLR-mediated nuclear factor kappa B (NF-κB) activation and cytokine and chemokine release, but also participates in NLR-C4 inflammasome activation. Taken together, our data confirm that Tim-3 signalling enhances injury after kidney IRI and demonstrated that Tim-3 is involved in regulating TLR-4/NF-κB signalling and NLR-C4 inflammasome activation, which provide evidence that Tim-3 signalling is critical for kidney IRI and may provide a new means to ameliorate kidney tissue immune responses in the clinics.
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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.