ArticleProceedings of the National Academy of Sciences of the United States of America2010
Cytokine-dependent but acquired immunity-independent arthritis caused by DNA escaped from degradation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 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
67 citing papers in PubMed, 101 citations in OpenAlex.
- Germinal-centre and extrafollicular B cell pathways in systemic lupus erythematosus.Nature reviews. Rheumatology · 2026Review
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- The lysosomal catabolism of nucleic acids-critical regulators of the innate immune system.Nucleic acids research · 2025Review
- Type I interferon-mediated autoinflammation in two unrelated patients due to a proximal intronic splice site variant inResearch square · 2025Article
- Innate Immune Receptors as Dynamic Modulators of Extrafollicular Autoimmune B Cell Response.Immunological reviews · 2025Review
- DNA-sensing pathways in health, autoinflammatory and autoimmune diseases.Nature immunology · 2024Review
- ZC3HAV1 facilitates STING activation and enhances inflammation.Communications biology · 2024Article
- Milk andAmerican journal of physiology. Gastrointestinal and liver physiology · 2024Article
- Efferocytosis: Current status and future prospects in the treatment of autoimmune diseases.Heliyon · 2024Review
- Cytoplasmic DNA and AIM2 inflammasome in RA: where they come from and where they go?Frontiers in immunology · 2024Review
- Immunomodulatory nano-preparations for rheumatoid arthritis.Drug delivery · 2023Review
- Oral vancomycin treatment suppresses gut trypsin activity and preserves intestinal barrier function during EAE.iScience · 2023Article
- Article
- STING-dependent interferon signatures restrict osteoclast differentiation and bone loss in mice.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- You are what you eat and how you digest it! A discussion on inflammatory efferocytosis.Frontiers in cell and developmental biology · 2023Review
- Absent in melanoma 2 (AIM2) in rheumatoid arthritis: novel molecular insights and implications.Cellular & molecular biology letters · 2022Review
- Intracellular Sensing of DNA in Autoinflammation and Autoimmunity.Arthritis & rheumatology (Hoboken, N.J.) · 2022Review
- Article
- Emerging Roles of the Innate Immune System Regulated by DNA Sensors in the Development of Vascular and Metabolic Diseases.Journal of atherosclerosis and thrombosis · 2022Review
- The Role of Interleukin 18/Interleukin 18-Binding Protein in Adult-Onset Still's Disease and Systemic Juvenile Idiopathic Arthritis.Journal of clinical medicine · 2022Review
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNase II digests the chromosomal DNA in macrophages after apoptotic cells and nuclei from erythroid precursors are engulfed. The DNase II-null mice develop a polyarthritis that resembles rheumatoid arthritis. Here, we showed that when bone marrow cells from the DNase II-deficient mice were transferred to the wild-type mice, they developed arthritis. A deficiency of Rag2 or a lack of lymphocytes accelerated arthritis of the DNase II-null mice, suggesting that the DNase II(-/-) macrophages were responsible for triggering arthritis, and their lymphocytes worked protectively. A high level of TNFα, IL-1β, and IL-6 was found in the affected joints of the DNase II-null mice, suggesting an inflammatory-skewed cytokine storm was established in the joints. A lack of TNFα, IL-1β, or IL-6 gene blocked the expression of the other cytokine genes as well and inhibited the development of arthritis. Neutralization of TNFα, IL-1β, or IL-6 had a therapeutic effect on the developed arthritis of the DNase II-null mice, indicating that the cytokine storm was essential for the maintenance of arthritis in the DNase II-deficient mice. Methotrexate, an antimetabolite that is often used to treat patients with rheumatoid arthritis, had a therapeutic effect with the DNase II-null mice. These properties of arthritis in the DNase II-null mice were similar to those found in human systemic-onset juvenile idiopathic arthritis or Still's disease, indicating that the DNase II-null mice are a good animal model of this type of arthritis.
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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.