ArticleThe Journal of experimental medicine1999
Monocyte chemoattractant protein 1-dependent leukocytic infiltrates are responsible for autoimmune disease in MRL-Fas(lpr) mice.
Article in The Journal of experimental medicine, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.
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Who cites it
98 citing papers in PubMed, 302 citations in OpenAlex.
- CCR2-overexpressing mesenchymal stromal cell-derived extracellular vesicles loaded with MPA ameliorate lupus nephritis.Journal of nanobiotechnology · 2026Article
- Vamifeport, a clinical stage oral ferroportin inhibitor, alleviates murine lupus nephritis: A pilot study.Clinical immunology (Orlando, Fla.) · 2026Article
- Engineered macrophage membrane-coated dihydroartemisinin nanoparticles with enhanced CCR2 expression improved symptoms in MRL/LPR mice by metabolic reprogramming of proinflammatory macrophages.Journal of translational medicine · 2025Article
- Podocyte, tubular epithelial-immune cell interplay in the pathogenesis of lupus nephritis.Frontiers in immunology · 2025Review
- Urinary biomarkers for active Lupus Nephritis that have survived independent validation across cohorts.Kidney international · 2024Review
- Unravelling monocyte functions: from the guardians of health to the regulators of disease.Discovery immunology · 2024Review
- Mesenchymal stem cells enhance CCL8 expression by podocytes in lupus-prone MRL.FasScientific reports · 2023Article
- Evaluation of the Involvement of Heme Oxygenase-1 Expression in Discoid Lupus Erythematosus Lesions.Antioxidants (Basel, Switzerland) · 2023Article
- Recent advances in cutaneous lupus.Journal of autoimmunity · 2022Review
- Monocytes transition to macrophages within the inflamed vasculature via monocyte CCR2 and endothelial TNFR2.The Journal of experimental medicine · 2022Article
- Gut dysbiosis is associated with acceleration of lupus nephritis.Scientific reports · 2022Article
- Serological, fragmentomic, and epigenetic characteristics of cell-free DNA in patients with lupus nephritis.Frontiers in immunology · 2022Article
- Biomarkers Associated with Organ-Specific Involvement in Juvenile Systemic Lupus Erythematosus.International journal of molecular sciences · 2021Review
- CDK4/6 inhibitor palbociclib reduces inflammation in lupus-prone mice.American journal of clinical and experimental urology · 2021Article
- Lymph node stromal CCL2 limits antibody responses.Science immunology · 2020Article
- Early and late neuropathological features of meningoencephalitis associated with Maraba virus infection.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2020Article
- Neuraminidase activity mediates IL-6 production by activated lupus-prone mesangial cells.American journal of physiology. Renal physiology · 2018Article
- Bim suppresses the development of SLE by limiting myeloid inflammatory responses.The Journal of experimental medicine · 2017Article
- The contribution of the programmed cell death machinery in innate immune cells to lupus nephritis.Clinical immunology (Orlando, Fla.) · 2017Review
- MCP-1-induced ERK/GSK-3β/Snail signaling facilitates the epithelial-mesenchymal transition and promotes the migration of MCF-7 human breast carcinoma cells.Cellular & molecular immunology · 2017Article
38 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Infiltrating leukocytes may be responsible for autoimmune disease. We hypothesized that the chemokine monocyte chemoattractant protein (MCP)-1 recruits macrophages and T cells into tissues that, in turn, are required for autoimmune disease. Using the MRL-Fas(lpr) strain with spontaneous, fatal autoimmune disease, we constructed MCP-1-deficient MRL-Fas(lpr) mice. In MCP-1-intact MRL-Fas(lpr) mice, macrophages and T cells accumulate at sites (kidney tubules, glomeruli, pulmonary bronchioli, lymph nodes) in proportion to MCP-1 expression. Deleting MCP-1 dramatically reduces macrophage and T cell recruitment but not proliferation, protects from kidney, lung, skin, and lymph node pathology, reduces proteinuria, and prolongs survival. Notably, serum immunoglobulin (Ig) isotypes and kidney Ig/C3 deposits are not diminished in MCP-1-deficient MRL-Fas(lpr) mice, highlighting the requirement for MCP-1-dependent leukocyte recruitment to initiate autoimmune disease. However, MCP-1-deficient mice are not completely protected from leukocytic invasion. T cells surrounding vessels with meager MCP-1 expression remain. In addition, downstream effector cytokines/chemokines are decreased in MCP-1-deficient mice, perhaps reflecting a reduction of cytokine-expressing leukocytes. Thus, MCP-1 promotes MRL-Fas(lpr) autoimmune disease through macrophage and T cell recruitment, amplified by increasing local cytokines/chemokines. We suggest that MCP-1 is a principal therapeutic target with which to combat autoimmune diseases.
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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.