ArticleMediators of inflammation2016
Kidney Expression of Toll Like Receptors in Lupus Nephritis: Quantification and Clinicopathological Correlations.
Article in Mediators of inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
- Tubulointerstitial inflammation in glomerular diseases: mechanistic pathways, prognostic value, and translational therapeutic targets.Renal failure · 2026Review
- Nucleic acid sensing pathways in kidney disease development.Nature reviews. Nephrology · 2026Review
- Renal macrophage TLR7 signaling in lupus nephritis: from pathogenic mechanisms to therapeutic opportunities.Frontiers in immunology · 2026Review
- The Expression of Toll-like Receptors (TLR7 and TLR9) in Class III and Class IV of Recently Diagnosed Lupus Nephritis with 12-Month Follow-Up.International journal of molecular sciences · 2024Article
- Interleukin-32 positive immune and resident cells in kidney samples from lupus patients: a pilot study.Frontiers in immunology · 2024Article
- Expression of interferon-stimulated gene 20 (ISG20), an antiviral effector protein, in glomerular endothelial cells: possible involvement of ISG20 in lupus nephritis.Renal failure · 2023Article
- CD8 T Cell-Derived Exosomal miR-186-5p Elicits Renal Inflammation via Activating Tubular TLR7/8 Signal Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Definitions, phenotypes, and subphenotypes in acute kidney injury-Moving towards precision medicine.Nephrology (Carlton, Vic.) · 2023Review
- Article
- Renal TLR-7/TNF-α pathway as a potential female-specific mechanism in the pathogenesis of autoimmune-induced hypertension.American journal of physiology. Heart and circulatory physiology · 2022Article
- Cell type-specific mechanistic target of rapamycin-dependent distortion of autophagy pathways in lupus nephritis.Translational research : the journal of laboratory and clinical medicine · 2022Review
- The innate immune system in human kidney inflammaging.Journal of nephrology · 2022Review
- Inhibitory effect of anti-malarial agents on the expression of proinflammatory chemokines via Toll-like receptor 3 signaling in human glomerular endothelial cells.Renal failure · 2021Article
- Toll-like Receptor Signaling Inhibitory Peptide Improves Inflammation in Animal Model and Human Systemic Lupus Erythematosus.International journal of molecular sciences · 2021Article
- Intravenous Administration of Toll-Like Receptor Inhibitory Peptide 1 is Effective for the Treatment of Systemic Lupus Erythematosus in aJournal of rheumatic diseases · 2021Article
- Review
- Toll-Like Receptors Regulate the Development and Progression of Renal Diseases.Kidney diseases (Basel, Switzerland) · 2021Review
- Toll-Like Receptor as a Potential Biomarker in Renal Diseases.International journal of molecular sciences · 2020Review
- TLR7 in B cells promotes renal inflammation and Gd-IgA1 synthesis in IgA nephropathy.JCI insight · 2020Article
- B cell-intrinsic TLR9 expression is protective in murine lupus.The Journal of clinical investigation · 2020Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective. The study aimed at locating and quantifying Toll Like Receptor (TLR) 3, 7, 8, and 9 expression in kidney of patients with lupus nephritis (LN) and correlating them with clinicopathological features. Methods. Kidney sections from 26 LN patients and 4 controls were analyzed by immunohistochemistry using anti-human TLR3, TLR7, TLR8, and TLR9 polyclonal antibodies; the number of TLR-positive nuclei/mm(2) was evaluated on digitalized images. Results. Compared to controls, LN showed a significantly higher amount of glomerular and tubulointerstitial TLR9 (p = 0.003 and p = 0.007), whole and tubulointerstitial TLR3 (p = 0.026 and p = 0.031), and a higher tubulointerstitial TLR7 (p = 0.022). TLR9 positively correlated with activity index (p = 0.0063) and tubular TLR7 with chronicity index (p = 0.026). TLR9 positively correlated with Renal-SLEDAI (p = 0.01). Conclusions. This is the first study quantifying kidney expressions of TLRs in LN patients; the results show an overexpression of TLR3, TLR7, and TLR9 and demonstrate a correlation with clinicopathological indices supporting a role of these mediators in the pathogenesis of LN.
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