ArticleJCI insight2018
Intracapillary immune complexes recruit and activate slan-expressing CD16+ monocytes in human lupus nephritis.
Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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.
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Who cites it
31 citing papers in PubMed, 44 citations in OpenAlex.
- The endothelium response to kidney injury.Nature reviews. Nephrology · 2026Review
- Regulatory Effects of CD14Journal of immunology research · 2026Article
- Cutaneous Lupus Features Specialized Stromal Niches and Altered Retroelement Expression.The Journal of investigative dermatology · 2025Article
- Wheat germ agglutinin-nanoparticles encapsulating itacitinib target and suppress pro-inflammatory slan+ monocytes.Nanomedicine (London, England) · 2025Article
- Breaking the cycle: immune complexes, complement activation, and novel immunotherapies in lupus nephritis.Frontiers in immunology · 2025Review
- Anti-PS IgG Immune Complexes Impair Macrophage Phagocytosis in SLE via LOX-Dependent Oxidative Stress.Journal of inflammation research · 2025Article
- Identification of cellular senescence-related genes as biomarkers for lupus nephritis based on bioinformatics.Frontiers in genetics · 2025Article
- Roles of macrophages in lupus nephritis.Frontiers in pharmacology · 2024Review
- A new generation of mesenchymal stromal/stem cells differentially trained by immunoregulatory probiotics in a lupus microenvironment.Stem cell research & therapy · 2023Article
- Pathogenic cellular and molecular mediators in lupus nephritis.Nature reviews. Nephrology · 2023Review
- Reduced peripheral blood dendritic cell and monocyte subsets in MDS patients with systemic inflammatory or dysimmune diseases.Clinical and experimental medicine · 2023Article
- NLRP12 is an innate immune checkpoint for repressing IFN signatures and attenuating lupus nephritis progression.The Journal of clinical investigation · 2023Article
- Immune complex-induced haptokinesis in human non-classical monocytes.Frontiers in immunology · 2023Article
- The role of lung-restricted autoantibodies in the development of primary and chronic graft dysfunction.Frontiers in transplantation · 2023Review
- Monocytes transition to macrophages within the inflamed vasculature via monocyte CCR2 and endothelial TNFR2.The Journal of experimental medicine · 2022Article
- Reduced frequencies and functional impairment of dendritic cell subsets and non-classical monocytes in myelodysplastic syndromes.Haematologica · 2022Article
- Endothelial cells: potential novel regulators of renal inflammation.American journal of physiology. Renal physiology · 2022Review
- Identification of a Novel Serum Proteomic Signature for Primary Sjögren's Syndrome.Frontiers in immunology · 2021Article
- Induction of NF-κB inflammatory pathway in monocytes by microparticles from patients with systemic lupus erythematosus.Heliyon · 2020Article
- IgG subclasses in cryoglobulins: link to composition and clinical manifestations.Arthritis research & therapy · 2020Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lupus nephritis is a major cause of morbidity in patients with systemic lupus erythematosus. Among the different types of lupus nephritis, intracapillary immune complex (IC) deposition and accumulation of monocytes are hallmarks of lupus nephritis class III and IV. The relevance of intracapillary ICs in terms of monocyte recruitment and activation, as well as the nature and function of these monocytes are not well understood. For the early focal form of lupus nephritis (class III) we demonstrate a selective accumulation of the proinflammatory population of 6-sulfo LacNAc+ (slan) monocytes (slanMo), which locally expressed TNF-α. Immobilized ICs induced a direct recruitment of slanMo from the microcirculation via interaction with Fc γ receptor IIIA (CD16). Interestingly, intravenous immunoglobulins blocked CD16 and prevented cell recruitment. Engagement of immobilized ICs by slanMo induced the production of neutrophil-attracting chemokine CXCL2 as well as TNF-α, which in a forward feedback loop stimulated endothelial cells to produce the slanMo-recruiting chemokine CX3CL1 (fractalkine). In conclusion, we observed that expression of CD16 equips slanMo with a unique capacity to orchestrate early IC-induced inflammatory responses in glomeruli and identified slanMo as a pathogenic proinflammatory cell type in lupus nephritis.
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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.