ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Roles of adipocytes and fibroblasts in activation of the alternative pathway of complement in inflammatory arthritis in mice.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
- Serum adipsin levels in rheumatic diseases: defining its role in disease activity and progression in rheumatoid arthritis and axial spondyloarthritis.Frontiers in immunology · 2025Article
- The Role of Adipsin, Complement Factor D, in the Pathogenesis of Graves' Orbitopathy.Investigative ophthalmology & visual science · 2023Article
- An estrogen-sensitive fibroblast population drives abdominal muscle fibrosis in an inguinal hernia mouse model.JCI insight · 2022Article
- The complex role of adipokines in obesity, inflammation, and autoimmunity.Clinical science (London, England : 1979) · 2021Review
- Dual Host-Intracellular Parasite Transcriptome of Enucleated Cells HostingInfection and immunity · 2020Article
- Key Components of the Complement Lectin Pathway Are Not Only Required for the Development of Inflammatory Arthritis but Also Regulate the Transcription of Factor D.Frontiers in immunology · 2020Article
- C2 IgM Natural Antibody Enhances Inflammation and Its Use in the Recombinant Single Chain Antibody-Fused Complement Inhibitor C2-Crry to Target Therapeutics to Joints Attenuates Arthritis in Mice.Frontiers in immunology · 2020Article
- Complement and its environmental determinants in the progression of human rheumatoid arthritis.Molecular immunology · 2019Article
- Review
- Complement in the Initiation and Evolution of Rheumatoid Arthritis.Frontiers in immunology · 2018Review
- Osteoarthritis and the Complement Cascade.Clinical medicine insights. Arthritis and musculoskeletal disorders · 2018Review
- Deconstructing the Lectin Pathway in the Pathogenesis of Experimental Inflammatory Arthritis: Essential Role of the Lectin Ficolin B and Mannose-Binding Protein-Associated Serine Protease 2.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Mannan-Binding Lectin-Associated Serine Protease 1/3 Cleavage of Pro-Factor D into Factor D In Vivo and Attenuation of Collagen Antibody-Induced Arthritis through Their Targeted Inhibition by RNA Interference-Mediated Gene Silencing.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Targeting mechanisms at sites of complement activation for imaging and therapy.Immunobiology · 2016Review
- Collectin-11 detects stress-induced L-fucose pattern to trigger renal epithelial injury.The Journal of clinical investigation · 2016Article
- Subsets of Visceral Adipose Tissue Nuclei with Distinct Levels of 5-Hydroxymethylcytosine.PloS one · 2016Article
- Complement activation in the context of stem cells and tissue repair.World journal of stem cells · 2015Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
The complement system is involved in mediation of joint damage in rheumatoid arthritis, with evidence suggesting activation of both the classical and alternative pathway (AP). The AP is both necessary and sufficient to mediate collagen Ab-induced arthritis, an experimental animal model of immune complex-induced joint disease. The AP in mice is dependent on MASP-1/3 cleavage of pro-factor D (pro-FD) into mature factor D (FD). The objectives of the current study were to determine the cells synthesizing MASP-1/3 and pro-FD in synovial tissue. Collagen Ab-induced arthritis was studied in wild-type C57BL/6 mice, and the localization of mRNA and protein for FD and MASP-1/3 in synovial adipose tissue (SAT) and fibroblast-like synoviocytes (FLS) was determined using various techniques, including laser capture microdissection. SAT was the sole source of mRNA for pro-FD. Cultured differentiated 3T3 adipocytes, a surrogate for SAT, produced pro-FD but no mature FD. FLS were the main source of MASP-1/3 mRNA and protein. Using cartilage microparticles (CMPs) coated with anti-collagen mAb and serum from MASP-1/3(-/-) mice as a source of factor B, pro-FD in 3T3 supernatants was cleaved into mature FD by MASP-1/3 in FLS supernatants. The mature FD was eluted from the CMP, and was not present in the supernatants from the incubation with CMP, indicating that cleavage of pro-FD into mature FD by MASP-1 occurred on the CMP. These results demonstrate that pathogenic activation of the AP can occur in the joint through immune complexes adherent to cartilage and the local production of necessary AP proteins by adipocytes and FLS.
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Registered trials
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