ArticleThe Journal of experimental medicine2007
A novel inhibitor of the alternative pathway of complement reverses inflammation and bone destruction in experimental arthritis.
Article in The Journal of experimental medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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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
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.
- Therapeutic Targeting of the Complement System: From Rare Diseases to Pandemics.Pharmacological reviews · 2021Pooled it
- Adventitial Niches, Complement and Inflammation in Pulmonary Vascular Disease: Current Status and Future Directions.Comprehensive Physiology · 2026Review
- Dynamic expression of complement receptor immunoglobulin (CRIg) on monocytes and its role in phagocytosis and killing of Staphylococcus aureus.Journal of biomedical science · 2026Article
- Complement C3 in panvascular disease: a central integrator of immune signaling and vascular remodeling.Clinical science (London, England : 1979) · 2025Review
- CG001, a C3b-targeted complement inhibitor, blocks 3 complement pathways: development and preclinical evaluation.Blood advances · 2024Article
- Whole blood transcriptomics reveals the enrichment of neutrophil activation pathways during erythema nodosum leprosum reaction.Frontiers in immunology · 2024Article
- New Insights into the Complement Receptor of the Ig Superfamily Obtained from Structural and Functional Studies on Two Mutants.ImmunoHorizons · 2023Article
- VSIG4 interaction with heparan sulfates inhibits VSIG4-complement binding.Glycobiology · 2023Article
- Immune checkpoints in rheumatoid arthritis: progress and promise.Frontiers in immunology · 2023Review
- Synovial tissue macrophages in joint homeostasis, rheumatoid arthritis and disease remission.Nature reviews. Rheumatology · 2022Review
- Immunomodulatory receptor VSIG4 is released during spontaneous bacterial peritonitis and predicts short-term mortality.JHEP reports : innovation in hepatology · 2022Article
- V-Set and immunoglobulin domain containing (VSIG) proteins as emerging immune checkpoint targets for cancer immunotherapy.Frontiers in immunology · 2022Review
- The role of C5a-C5aR1 axis in bone pathophysiology: A mini-review.Frontiers in cell and developmental biology · 2022Review
- Neutrophils Require Activation to Express Functional Cell-Surface Complement Receptor Immunoglobulin.Frontiers in immunology · 2022Article
- CRIg on liver macrophages clears pathobionts and protects against alcoholic liver disease.Nature communications · 2021Article
- Halting targeted and collateral damage to red blood cells by the complement system.Seminars in immunopathology · 2021Review
- B7 Family Molecule VSIG4 Regulates Intestinal Anti-Microorganisms · 2021Article
- Complement Receptors and Their Role in Leukocyte Recruitment and Phagocytosis.Frontiers in cell and developmental biology · 2021Review
- Article
- Therapeutic Lessons to be Learned From the Role of Complement Regulators as Double-Edged Sword in Health and Disease.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Complement is an important component of the innate and adaptive immune response, yet complement split products generated through activation of each of the three complement pathways (classical, alternative, and lectin) can cause inflammation and tissue destruction. Previous studies have shown that complement activation through the alternative, but not classical, pathway is required to initiate antibody-induced arthritis in mice, but it is unclear if the alternative pathway (AP) plays a role in established disease. Previously, we have shown that human complement receptor of the immunoglobulin superfamily (CRIg) is a selective inhibitor of the AP of complement. Here, we present the crystal structure of murine CRIg and, using mutants, provide evidence that the structural requirements for inhibition of the AP are conserved in human and mouse. A soluble form of CRIg reversed inflammation and bone loss in two experimental models of arthritis by inhibiting the AP of complement in the joint. Our data indicate that the AP of complement is not only required for disease induction, but also disease progression. The extracellular domain of CRIg thus provides a novel tool to study the effects of inhibiting the AP of complement in established disease and constitutes a promising therapeutic with selectivity for a single complement pathway.
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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.