Rheumatoid arthritis and the complement system
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Summary
It appears that anaphylatoxin C5a is the main product of complement activation responsible for tissue damage in RA although deposition of membrane attack complex as well as opsonization with fragments of C3b are also important.
- Type
- article
- Published
- 2007-01-01
- Cited by
- 200
- References
- 191
- Access
- Open access
- OpenAlex
- https://openalex.org/W17852027
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:24958329
Keywords
Computer science
References
- A Role for Complement in Antibody-Mediated Inflammation: C5-Deficient DBA/1 Mice Are Resistant to Collagen-Induced Arthritis
- Genetic control of collagen‐induced arthritis in a cross with NOD and C57BL/10 mice is dependent on gene regions encoding complement factor 5 and FcγRIIb and is not associated with loci controlling diabetes
- Transmission of antibody‐induced arthritis is independent of complement component 4 (C4) and the complement receptors 1 and 2 (CD21/35)
- Mannose‐binding lectin engagement with late apoptotic and necrotic cells
- Drug evaluation: the C5a receptor antagonist PMX-53.
- Complement activation and immune complexes in children with polyarticular juvenile rheumatoid arthritis: a longitudinal study.
- Complement. Second of two parts.
- Two edged role of mannose binding lectin in rheumatoid arthritis: a cross sectional study.
- Measurement of terminal complement complexes in rheumatoid arthritis.
- Terminal complement complex in synovial tissue from patients affected by rheumatoid arthritis, osteoarthritis and acute joint trauma.
- A collagen‐binding 59‐kd protein (fibromodulin) is structurally related to the small interstitial proteoglycans PG‐S1 and PG‐S2 (decorin).
- Human rheumatoid synovial cell stimulation by the membrane attack complex and other pore-forming toxins in vitro: the role of calcium in cell activation.
- Complement. First of two parts.
- Functional significance of the subunits of carboxypeptidase N (kininase I).
- Substances reactive with mannose-binding protein (MBP) in sera of patients with rheumatoid arthritis.
- Biosynthesis of complement.
- Characterization of a soluble form of the C3b/C4b receptor (CR1) in human plasma.
- Biology of fibrocartilage cells.
- The proteoglycan decorin binds C1q and inhibits the activity of the C1 complex.
- The Differing Roles of the Classical and Mannose-Binding Lectin Complement Pathways in the Events following Skeletal Muscle Ischemia-Reperfusion1
Cited by
- NC4 Domain of Cartilage-specific Collagen IX Inhibits Complement Directly Due to Attenuation of Membrane Attack Formation and Indirectly through Binding and Enhancing Activity of Complement Inhibitors C4B-binding Protein and Factor H*
- Role of Complement on Broken Surfaces After Trauma.
- Complement in therapy and disease: Regulating the complement system with antibody-based therapeutics.
- The role of citrullination in the development of mouse and human inflammatory arthritis
- Complement autoantibodies in atypical haemolytic uraemic syndrome and IgA nephropathy
- Complement factor H dysfunction in atypical hemolytic uremic syndrome
- Review on complement analysis method and the roles of glycosaminoglycans in the complement system.
- Inflammation and Complement Activation in Intracranial Artery Aneurysms
- M-ficolin levels reflect disease activity and predict remission in early rheumatoid arthritis.
- Chondroitin sulfate and abnormal contact system in rheumatoid arthritis.
- Interleukin 17 contributes to the chronicity of inflammatory diseases such as rheumatoid arthritis
- The major risk alleles of age‐related macular degeneration (AMD) in CFH do not play a major role in rheumatoid arthritis (RA)
- Complement-targeted therapeutics in periodontitis
- Fcγ and Complement Receptors and Complement Proteins in Neutrophil Activation in Rheumatoid Arthritis: Contribution to Pathogenesis and Progression and Modulation by Natural Products
- Suppression of antibody‐mediated arthritis in mice by Fab fragments of the mediating antibodies
- How complement activation influences the development of chronic synovitis in a mouse model of rheumatoid arthritis
- Complement in Disease - Extracellular Proteins as Complement Regulators
- IgM and IgA Rheumatoid Factors Purified from Rheumatoid Arthritis Sera Boost the Fc Receptor– and Complement-Dependent Effector Functions of the Disease-Specific Anti–Citrullinated Protein Autoantibodies
- Role of the Receptor for the Globular Domain of C1q Protein in the Pathogenesis of HCV-Related Cryoglobulin Vascular Damage
- Ficolin Gene Polymorphisms in Systemic Lupus Erythematosus and Rheumatoid Arthritis
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