ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Essential role of surface-bound complement factor H in controlling immune complex-induced arthritis.
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 16 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- The evolving landscape of complement therapeutics in rheumatology.Annals of the rheumatic diseases · 2026Review
- Regulation of the innate immune response in rheumatoid arthritis.Frontiers in immunology · 2025Review
- Analysis of Complement Gene Expression, Clinical Associations, and Biodistribution of Complement Proteins in the Synovium of Early Rheumatoid Arthritis Patients Reveals Unique Pathophysiologic Features.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Characterization of Binding Properties of Individual Functional Sites of Human Complement Factor H.Frontiers in immunology · 2020Article
- The human complement receptor type 2 (CR2)/CR1 fusion protein TT32, a novel targeted inhibitor of the classical and alternative pathway C3 convertases, prevents arthritis in active immunization and passive transfer mouse models.Molecular immunology · 2019Article
- Targeting IgG in Arthritis: Disease Pathways and Therapeutic Avenues.International journal of molecular sciences · 2018Review
- Complement in the Initiation and Evolution of Rheumatoid Arthritis.Frontiers in immunology · 2018Review
- The Murine Factor H-Related Protein FHR-B Promotes Complement Activation.Frontiers in immunology · 2017Article
- Properdin: a tightly regulated critical inflammatory modulator.Immunological reviews · 2016Review
- Properdin-Mediated C5a Production Enhances Stable Binding of Platelets to Granulocytes in Human Whole Blood.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Targeting mechanisms at sites of complement activation for imaging and therapy.Immunobiology · 2016Review
- Complement Regulator FHR-3 Is Elevated either Locally or Systemically in a Selection of Autoimmune Diseases.Frontiers in immunology · 2016Article
- New insights into disease-specific absence of complement factor H related protein C in mouse models of spontaneous autoimmune diseases.Molecular immunology · 2014Article
- Identification of a novel mode of complement activation on stimulated platelets mediated by properdin and C3(H2O).Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Roles of adipocytes and fibroblasts in activation of the alternative pathway of complement in inflammatory arthritis in mice.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Human C3 glomerulopathy provides unique insights into complement factor H-related protein function.The Journal of clinical investigation · 2013Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Factor H (fH) is an endogenous negative regulator of the alternative pathway (AP) that binds polyanions as well as complement activation fragments C3b and C3d. The AP is both necessary and sufficient to develop collagen Ab-induced arthritis (CAIA) in mice; the mechanisms whereby normal control of the AP is overcome and injury develops are unknown. Although primarily a soluble circulating protein, fH can also bind to tissues in a manner dependent on the carboxyl-terminal domain containing short consensus repeats 19 and 20. We examined the role of fH in CAIA by blocking its binding to tissues through administration of a recombinant negative inhibitor containing short consensus repeats 19 and 20 (rfH19-20), which impairs fH function and amplifies surface AP activation in vitro. Administration of rfH19-20, but not control rfH3-5, significantly worsened clinical disease activity, histopathologic injury, and C3 deposition in the synovium and cartilage in wild-type and fH(+/-) mice. In vitro studies demonstrated that rfH19-20 increased complement activation on cartilage extracts and injured fibroblast-like synoviocytes, two major targets of complement deposition in the joint. We conclude that endogenous fH makes a significant contribution to inhibition of the AP in CAIA through binding to sites of immune complex formation and complement activation.
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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.