ArticleThe Journal of clinical investigation2019
Patrolling monocytes promote the pathogenesis of early lupus-like glomerulonephritis.
Article in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 96 citations in OpenAlex.
- The SLC15A4-TASL complex is essential for lupus development in mice.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- The endothelium response to kidney injury.Nature reviews. Nephrology · 2026Review
- Identification of Lupus Immune Complex-Driven Pathogenic Pro-inflammatory Monocytes and Macrophages in Systemic Lupus Erythematosus.bioRxiv : the preprint server for biology · 2026Article
- The sex-biased chromatin modifier SMC1A promotes autoimmunity by shaping inflammatory pathways in patients with SLE.Nature communications · 2025Article
- Circulating Cathepsin D Exacerbates Injury-Induced Brain Damage by Promoting Neutrophil Infiltration Into the Brain.Journal of the American Heart Association · 2025Article
- A human-mouse atlas of intrarenal myeloid cells identifies conserved disease-associated macrophages in lupus nephritis.The Journal of experimental medicine · 2025Article
- Lupus nephritis.Nature reviews. Disease primers · 2025Review
- Article
- Role of STING Deficiency in Amelioration of Mouse Models of Lupus and Atherosclerosis.Arthritis & rheumatology (Hoboken, N.J.) · 2025Article
- M1 and M2 Macrophage Polarization Correlates with Activity and Chronicity Indices in Lupus Nephritis.Life (Basel, Switzerland) · 2025Article
- Myeloid cells as IFNα producers in systemic lupus erythematosus.Frontiers in immunology · 2025Review
- Identification of cellular senescence-related genes as biomarkers for lupus nephritis based on bioinformatics.Frontiers in genetics · 2025Article
- The path ahead for understanding Toll-like receptor-driven systemic autoimmunity.Current opinion in immunology · 2024Review
- Critical Analysis of Cytoplasmic Progression of Inflammatory Signaling Suggests Potential Pharmacologic Targets for Wound Healing and Fibrotic Disorders.Biomedicines · 2024Review
- Article
- Mechanisms underlying aryl hydrocarbon receptor-driven divergent macrophage function.Toxicological sciences : an official journal of the Society of Toxicology · 2024Review
- Immune cell signatures and inflammatory mediators: unraveling their genetic impact on chronic kidney disease through Mendelian randomization.Clinical and experimental medicine · 2024Article
- Monocytes and Macrophages in Kidney Disease and Homeostasis.International journal of molecular sciences · 2024Review
- Roles of macrophages in lupus nephritis.Frontiers in pharmacology · 2024Review
- Transcobalamin 2 orchestrates monocyte proliferation and TLR4-driven inflammation in systemic lupus erythematosus via folate one-carbon metabolism.Frontiers in immunology · 2024Article
4 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Systemic lupus erythematosus (SLE) is a complex autoimmune disease with genetic and environmental contributions. Hallmarks of the disease are the appearance of immune complexes (IC) containing autoreactive Abs and TLR-activating nucleic acids, whose deposition in kidney glomeruli is suspected to promote tissue injury and glomerulonephritis (GN). Here, using a mouse model based on the human SLE susceptibility locus TNFAIP3-interacting protein 1 (TNIP1, also known as ABIN1), we investigated the pathogenesis of GN. We found that GN was driven by TLRs but, remarkably, proceeded independently of ICs. Rather, disease in 3 different mouse models and patients with SLE was characterized by glomerular accumulation of patrolling monocytes (PMos), a cell type with an emerging key function in vascular inflammation. Consistent with such function in GN, monocyte-specific deletion of ABIN1 promoted kidney disease, whereas selective elimination of PMos provided protection. In contrast to GN, PMo elimination did not protect from reduced survival or disease symptoms such as IC generation and splenomegaly, suggesting that GN and other inflammatory processes are governed by distinct pathogenic mechanisms. These data identify TLR-activated PMos as the principal component of an intravascular process that contributes to glomerular inflammation and kidney injury.
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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.