ArticleAmerican journal of physiology. Renal physiology2018
Intrarenal Toll-like receptor 4 and Toll-like receptor 2 expression correlates with injury in antineutrophil cytoplasmic antibody-associated vasculitis.
Article in American journal of physiology. Renal physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Review
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- Gene therapy enhances deoxyribonuclease I treatment in antimyeloperoxidase glomerulonephritis.JCI insight · 2025Article
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- Damage-Associated Molecular Patterns and Pattern Recognition Receptors in the Podocyte.Journal of the American Society of Nephrology : JASN · 2025Review
- Transcriptome Analysis of BAFF/BAFF-R System in Murine Nephrotoxic Serum Nephritis.International journal of molecular sciences · 2024Article
- Unravelling the Link between the Gut Microbiome and Autoimmune Kidney Diseases: A Potential New Therapeutic Approach.International journal of molecular sciences · 2024Review
- Circulating cold-inducible RNA-binding protein levels in microscopic polyangiitis and granulomatosis with polyangiitis : Correlation with disease activity.Zeitschrift fur Rheumatologie · 2024Article
- Article
- Novel Therapies for ANCA-associated Vasculitis: Apilimod Ameliorated Endothelial Cells Injury through TLR4/NF-κB Pathway and NLRP3 Inflammasome.Current pharmaceutical design · 2024Article
- Identification of potential biomarkers and therapeutic targets for antineutrophil cytoplasmic antibody-associated glomerulonephritis.iScience · 2023Article
- Serum calprotectin and renal function decline in ANCA-associated vasculitides: a post hoc analysis of MAINRITSAN trial.RMD open · 2023Article
- Review
- Article
- Identification and validation of immune-associated NETosis subtypes and biomarkers in anti-neutrophil cytoplasmic antibody associated glomerulonephritis.Frontiers in immunology · 2023Article
- The innate immune system in human kidney inflammaging.Journal of nephrology · 2022Review
- Danger-associated molecular pattern molecules and the receptor for advanced glycation end products enhance ANCA-induced responses.Rheumatology (Oxford, England) · 2022Article
- Regulatory role and mechanisms of myeloid TLR4 in anti-GBM glomerulonephritis.Cellular and molecular life sciences : CMLS · 2021Article
- The Emerging Role of Innate Immunity in Chronic Kidney Diseases.International journal of molecular sciences · 2020Review
- Animal Models of ANCA Associated Vasculitis.Frontiers in immunology · 2020Review
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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
In antineutrophil cytoplasmic antibody-associated vasculitis (AAV), Toll-like receptors (TLRs) may be engaged by infection-associated patterns and by endogenous danger signals, linking infection and innate inflammation with this autoimmune disease. This study examined intrarenal TLR2, TLR4, and TLR9 expression and renal injury in AAV, testing the hypothesis that increased TLR expression correlates with renal injury. Patients with AAV exhibited both glomerular and tubulointerstitial expression of TLR2, TLR4, and TLR9, with TLR4 being the most prominent in both compartments. Glomerular TLR4 expression correlated with glomerular segmental necrosis and cellular crescents, with TLR2 expression correlating with glomerular segmental necrosis. The extent and intensity of glomerular and tubulointerstitial TLR4 expression and the intensity of glomerular TLR2 expression inversely correlated with the presenting estimated glomerular filtration rate. Although myeloid cells within the kidney expressed TLR2, TLR4, and TLR9, TLR2 and TLR4 colocalized with endothelial cells and podocytes, whereas TLR9 was expressed predominantly by podocytes. The functional relevance of intrarenal TLR expression was further supported by the colocalization of TLRs with their endogenous ligands high-mobility group box 1 and fibrinogen. Therefore, in AAV, the extent of intrarenal TLR4 and TLR2 expression and their correlation with renal injury indicates that TLR4, and to a lesser degree TLR2, may be potential therapeutic targets in this disease.
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