ReviewClinical reviews in allergy & immunology2011
Toll-like receptors and lupus nephritis.
Review in Clinical reviews in allergy & immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- A meta-analysis of public microarray data identifies gene regulatory pathways deregulated in peripheral blood mononuclear cells from individuals with Systemic Lupus Erythematosus compared to those without.BMC medical genomics · 2016Pooled it
- Long non-coding RNA in IgA nephropathy: a comprehensive review.Renal failure · 2025Review
- Molecular Differences in Glomerular Compartment to Distinguish Immunoglobulin A Nephropathy and Lupus Nephritis.Journal of inflammation research · 2024Article
- Association of Immune-Related Genetic and Epigenetic Alterations with Lupus Nephritis.Kidney diseases (Basel, Switzerland) · 2022Review
- Review
- Mycophenolic acid, the active form of mycophenolate mofetil, interferes with IRF7 nuclear translocation and type I IFN production by plasmacytoid dendritic cells.Arthritis research & therapy · 2020Article
- Review
- FcγRIIIa Signaling Modulates Endosomal TLR Responses in Human CD4Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Association between Staphylococcus aureus nasal carriage and disease phenotype in patients affected by systemic lupus erythematosus.Arthritis research & therapy · 2016Article
- FcγRIIIa-Syk Co-signal Modulates CD4+ T-cell Response and Up-regulates Toll-like Receptor (TLR) Expression.The Journal of biological chemistry · 2016Article
- Kidney Expression of Toll Like Receptors in Lupus Nephritis: Quantification and Clinicopathological Correlations.Mediators of inflammation · 2016Article
- Systemic Lupus Erythematosus: Old and New Susceptibility Genes versus Clinical Manifestations.Current genomics · 2014Article
- The role of disease activity score 28 in the evaluation of articular involvement in systemic lupus erythematosus.TheScientificWorldJournal · 2014Article
- High prevalence of antinuclear antibodies in children with thyroid autoimmunity.Journal of immunology research · 2014Article
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A variety of immune mechanisms, both humoral and cellular, are involved in the onset and amplification of the inflammatory response in lupus nephritis (LN). Accumulating evidence substantiates the view that innate immunity pathways may also amplify inflammatory reactions within the kidneys. Toll-like receptors (TLRs) are essential modulators of the innate immune response thanks to their ability to rocognize conserved molecular patterns that are microbe specific and other danger signals. Their recognition of endogenous molecules released from injured cells may also contribute to renal inflammation. Studies conducted in vivo and in vitro provide experimental evidence for the functional role of TLRs in LN. Intriguingly, these data suggest that pharmacological TLR signal suppression could be a useful approach to the treatment of systemic lupus erythematosus.
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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.