ArticleThe Journal of clinical investigation2004
Experimental arthritis in CC chemokine receptor 2-null mice closely mimics severe human rheumatoid arthritis.
Article in The Journal of clinical investigation, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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
46 citing papers in PubMed, 127 citations in OpenAlex.
- Expanding horizons in theragnostics: from oncology to multidisciplinary applications.La Radiologia medica · 2025Review
- Transcriptomic insights into early mechanisms underlying post-chikungunya chronic inflammatory joint disease.Scientific reports · 2025Article
- CC-Chemokine Receptor-2 Expression in Osteoblasts Contributes to Cartilage and Bone Damage during Post-Traumatic Osteoarthritis.Biomolecules · 2023Article
- Inactivation of the gene encoding procalcitonin prevents antibody-mediated arthritis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Scale down and optimized automated production of [68Ga]68Ga-DOTA-ECL1i PET tracer targeting CCR2 expression.EJNMMI radiopharmacy and chemistry · 2023Article
- Chemokines and chemokine receptors as promising targets in rheumatoid arthritis.Frontiers in immunology · 2023Review
- Early ablation of Ccr2 in aggrecan-expressing cells following knee injury ameliorates joint damage and pain during post-traumatic osteoarthritis.Osteoarthritis and cartilage · 2022Article
- Soluble CCR2 gene therapy controls joint inflammation, cartilage damage, and the progression of osteoarthritis by targeting MCP-1 in a monosodium iodoacetate (MIA)-induced OA rat model.Journal of translational medicine · 2022Article
- Assessment of mesenchymal stem/stromal cell-based therapy in K/BxN serum transfer-induced arthritis.Frontiers in immunology · 2022Article
- PET Imaging Radiotracers of Chemokine Receptors.Molecules (Basel, Switzerland) · 2021Review
- Review
- Non-classical monocytes as mediators of tissue destruction in arthritis.Annals of the rheumatic diseases · 2018Article
- CCR2 deficiency does not provide sustained improvement of muscular dystrophy in mdx5cv mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Macrophage heterogeneity in the context of rheumatoid arthritis.Nature reviews. Rheumatology · 2016Review
- Inflammatory Cell Migration in Rheumatoid Arthritis: A Comprehensive Review.Clinical reviews in allergy & immunology · 2016Review
- Effects of VLA-1 Blockade on Experimental Inflammation in Mice.The Kobe journal of medical sciences · 2016Article
- Myeloid-derived suppressor cells regulate T cell and B cell responses during autoimmune disease.Journal of leukocyte biology · 2015Article
- Mechanisms of tissue damage in arthritis.Seminars in immunopathology · 2014Review
- CCR2 deficiency promotes exacerbated chronic erosive neutrophil-dominated chikungunya virus arthritis.Journal of virology · 2014Article
- Important role of CCR2 in a murine model of coronary vasculitis.BMC immunology · 2012Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
The prevailing paradigm is that in human rheumatoid arthritis (RA), the accumulation of monocytes and T cells in the joint, mediated in part by such CC chemokine receptors (CCRs) as CCR2 and CCR5, respectively, plays a central role in disease pathogenesis. To further validate this paradigm, we conducted proof-of-principle studies and tested the hypothesis that gene inactivation of Ccr2 or Ccr5 will ameliorate experimental RA. Contrary to our expectations, we found that in two well-established murine models of experimental RA, CCR2 expression in the hematopoietic cell compartment served as a negative regulator of autoantibody production as well as arthritic disease onset, severity, and resolution. In contrast, the RA phenotype in Ccr5-null mice was similar to that of WT mice. Remarkably, the collagen-induced arthritis phenotype of Ccr2-/- mice mimicked closely that of severe human RA, including production of rheumatoid factor, enhanced T cell production, and monocyte/macrophage accumulation in the joints. Our findings demonstrate an essential protective role of CCR2 expression in RA, indicate the existence of alternative receptors responsible for monocyte/macrophage accumulation to inflamed joints, and emphasize the need to clarify carefully the complex effects of the chemokine system in RA before they can be considered as therapeutic targets.
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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.