ArticleMolecular immunology2019
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.
Article in Molecular immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 24 citations in OpenAlex.
- Bioorthogonal tuning of nanosurface opsonisationChemical communications (Cambridge, England) · 2026Article
- Enhanced immunocompatibility and hemocompatibility of nanomedicines across multiple species using complement pathway inhibitors.Science advances · 2025Article
- Identifying Therapeutic Targets and Potential Drugs for Diabetic Retinopathy: Focus on Oxidative Stress and Immune Infiltration.Journal of inflammation research · 2025Article
- Complement propagates visual system pathology following traumatic brain injury.Journal of neuroinflammation · 2024Article
- Decay-Accelerating Factor Differentially Associates With Complement-Mediated Damage in Synovium After Meniscus Tear as Compared to Anterior Cruciate Ligament Injury.Immune network · 2024Article
- Inhibition of acute complement responses towards bolus-injected nanoparticles using targeted short-circulating regulatory proteins.Nature nanotechnology · 2024Article
- Targeted complement inhibition using bispecific antibodies that bind local antigens and endogenous complement regulators.Frontiers in immunology · 2024Article
- 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
- 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
- Antibody-Dependent Complement Responses toward SARS-CoV-2 Receptor-Binding Domain Immobilized on "Pseudovirus-like" Nanoparticles.ACS nano · 2022Article
- Development and Optimization of Bifunctional Fusion Proteins to Locally Modulate Complement Activation in Diseased Tissue.Frontiers in immunology · 2022Article
- Complement Inhibitors Block Complement C3 Opsonization and Improve Targeting Selectivity of Nanoparticles in Blood.Bioconjugate chemistry · 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
- 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
- Combining MAP-1:CD35 or MAP-1:CD55 fusion proteins with pattern-recognition molecules as novel targeted modulators of the complement cascade.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
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Authors and funding
14 authors at 2 institutions in 1 country.
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Abstract
Complement activation in human diseases is characterized by the local covalent deposition of the long-lived C3 fragments iC3b/C3dg/C3d. Previously, TT30, a complement alternative pathway (AP)-selective inhibitor, was designed as a fusion protein linking the first four short consensus repeats (SCRs) of human complement receptor type 2 (CR2) with the first five SCRs of human factor H (fH). TT30 acts by utilizing CR2 SCR1-4 to bind the initially formed iC3b/C3dg/C3d fragments and delivering surface-targeted inhibition of AP C3 and C5 convertases through fH SCR 1-5. In order to combine classical (CP) and lectin (LP) pathway inhibitory abilities employing CR2-mediated targeting, TT32 was developed. TT32 is a CR2-CR1 fusion protein using the first ten SCRs of CR1, chosen because they contain both C3 and C5 convertase inhibitory activity through utilization of decay-acceleration and cofactor activity for both AP and CP. In Wieslab assays, TT32 showed potent inhibition of the CP and AP with IC
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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.