ArticleFrontiers in immunology2020
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.
Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Article
- Complement activation targeted inhibitor C2-FH ameliorates acetaminophen-induced liver injury in mice.World journal of hepatology · 2024Article
- A single-chain antibody construct with specificity of a natural IgM antibody reduces hepatic ischemia reperfusion injury in mice.Journal of cellular and molecular medicine · 2024Article
- Highly pathogenic natural monoclonal antibody B4-IgM recognizes a post-translational modification comprised of acetylated N-terminal methionine followed by aspartic or glutamic acid.Molecular immunology · 2023Article
- Expression dynamics of Crry at the implantation sites in normal pregnancy and response against miscarriage induction.The Journal of veterinary medical science · 2023Article
- Potential causal role of synovial complement system activation in the development of post-traumatic osteoarthritis after anterior cruciate ligament injury or meniscus tear.Frontiers in immunology · 2023Article
- Complement Inhibition Targeted to Injury Specific Neoepitopes Attenuates Atherogenesis in Mice.Frontiers in cardiovascular medicine · 2021Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Natural IgM antibodies (NAbs) have been shown to recognize injury-associated neoepitopes and to initiate pathogenic complement activation. The NAb termed C2 binds to a subset of phospholipids displayed on injured cells, and its role(s) in arthritis, as well as the potential therapeutic benefit of a C2 NAb-derived ScFv-containing protein fused to a complement inhibitor, complement receptor-related y (Crry), on joint inflammation are unknown. Our first objective was to functionally test mAb C2 binding to apoptotic cells from the joint and also evaluate its inflammation enhancing capacity in collagen antibody-induced arthritis (CAIA). The second objective was to generate and test the complement inhibitory capacity of C2-Crry fusion protein in the collagen-induced arthritis (CIA) model. The third objective was to demonstrate
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Registered trials
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