ArticleJournal of autoimmunity2019
NF-kB signaling in myeloid cells mediates the pathogenesis of immune-mediated nephritis.
Article in Journal of autoimmunity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
- CCR2-overexpressing mesenchymal stromal cell-derived extracellular vesicles loaded with MPA ameliorate lupus nephritis.Journal of nanobiotechnology · 2026Article
- Stress-Dependent NF-κB Signaling in Acute Kidney Injury: Linking Inflammation, Autophagy, and Apoptosis.International journal of molecular sciences · 2026Review
- Application of the nephrotoxic serum nephritis model in glomerulonephritis research.Molecular medicine (Cambridge, Mass.) · 2026Review
- NF-κB-driven lymphangiogenesis affects kidney function via a VEGFR-3-mediated pathway.JCI insight · 2026Article
- NF-κB in inflammation and cancer.Cellular & molecular immunology · 2025Review
- The path less traveled: the non-canonical NF-κB pathway in systemic lupus erythematosus.Frontiers in immunology · 2025Review
- Lang-chuang-ding restores bone homeostasis in systemic lupus erythematosus associated osteoporosis by targeting NF-κB signaling: a network pharmacology and experimental study.Frontiers in endocrinology · 2025Article
- NF-κB in biology and targeted therapy: new insights and translational implications.Signal transduction and targeted therapy · 2024Review
- Pathogenic cellular and molecular mediators in lupus nephritis.Nature reviews. Nephrology · 2023Review
- Role of vascular endothelial growth factor B in nonalcoholic fatty liver disease and its potential value.World journal of hepatology · 2023Review
- The Roles of TRAF3 in Immune Responses.Disease markers · 2023Review
- The anti-inflammatory activity of GABA-enrichedFrontiers in nutrition · 2023Article
- Novel loss-of-function mutations inClinical kidney journal · 2022Article
- The CD6/ALCAM pathway promotes lupus nephritis via T cell-mediated responses.The Journal of clinical investigation · 2022Article
- Molecular Taxonomy of Systemic Lupus Erythematosus Through Data-Driven Patient Stratification: Molecular Endotypes and Cluster-Tailored Drugs.Frontiers in immunology · 2022Article
- Treatment of Lupus Nephritis from Iranian Traditional Medicine and Modern Medicine Points of View: A Comparative Study.Evidence-based complementary and alternative medicine : eCAM · 2021Review
- IL-38: A novel cytokine in systemic lupus erythematosus pathogenesis.Journal of cellular and molecular medicine · 2020Article
- Aliskiren improves renal morphophysiology and inflammation in Wistar rats with 2K1C renovascular hypertension.Histology and histopathology · 2020Article
- IFN-BioMed research international · 2020Article
- Type I interferons and endoplasmic reticulum stress in health and disease.International review of cell and molecular biology · 2020Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Immune-mediated glomerulonephritis is a serious end organ pathology that commonly affects patients with systemic lupus erythematosus (SLE). A classic murine model used to study lupus nephritis (LN) is nephrotoxic serum nephritis (NTN), in which mice are passively transferred nephrotoxic antibodies. We have previously shown that macrophages are important in the pathogenesis of LN. To further investigate the mechanism by which macrophages contribute to the pathogenic process, and to determine if this contribution is mediated by NF-κB signaling, we created B6 mice which had RelA knocked out in myeloid cells, thus inhibiting classical NF-κB signaling in this cell lineage. We induced NTN in this strain to assess the importance of macrophage derived NF-κB signaling in contributing to disease progression. Myeloid cell RelA knock out (KO) mice injected with nephrotoxic serum had significantly attenuated proteinuria, lower BUN levels, and improved renal histopathology compared to control injected wildtype B6 mice (WT). Inhibiting myeloid NF-κB signaling also decreased inflammatory modulators within the kidneys. We found significant decreases of IL-1a, IFNg, and IL-6 in kidneys from KO mice, but higher IL-10 expression. Flow cytometry revealed decreased numbers of kidney infiltrating classically activated macrophages in KO mice as well. Our results indicate that macrophage NF-κB signaling is instrumental in the contribution of this cell type to the pathogenesis of NTN. While approaches which decrease macrophage numbers can be effective in immune mediated nephritis, more targeted treatments directed at modulating macrophage signaling and/or function could be beneficial, at least in the early stages of disease.
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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.