Activation of complement components C3 and factor B in synovial fluids. 1977

G G Hunder, and F C McDuffie, and B J Mullen

Synovial fluids from 106 patients with various types of arthritis were examined for the presence of conversion products of C3 by means of crossed antigen-antibody electrophoresis and for products of factor B by immunoelectrophoresis. C3 conversion was found in all 15 fluids from patients with seropositive rheumatoid arthritis, in 11 of 15 with seronegative rheumatoid arthritis, in the majority with probable and possible rheumatoid arthritis, juvenile rheumatoid arthritis, SLE, pseudogout, gout, Reiter's syndrome, and frequently in other arthritides studied, but in only one of 15 with degenerative arthritis. In 53 synovial fluids a single C3 conversion peak was seen in addition to the native protein and in 18 others two conversion peaks were present. In many synovial fluids showing conversion whole-complement titers and C3 protein concentrations were normal. In both rheumatoid arthritis and crystal synovitis the per cent of C3 conversion, as estimated by planimetry, correlated with synovial fluid leukocyte counts, Factor B conversion was found in 31 fluids and usually occurred in fluids also showing C3 conversion. The findings indicate that in vivo activation of components of the classical and alternative considered mediated by immune complexes. Activation is also commonly present in a wide variety of other inflammatory arthritides and ofter would not be recognized by measuring only concentrations of hemolytic whole complement or C3 by immunodiffusion. The positive association between C3 conversion and synovial fluid polymorphonuclear leukocytes suggests that chemotactic factors generated from complement may be responsible for the attraction of leukocytes into the synovial space in these diseases.

UI MeSH Term Description Entries
D007122 Immunoelectrophoresis A technique that combines protein electrophoresis and double immunodiffusion. In this procedure proteins are first separated by gel electrophoresis (usually agarose), then made visible by immunodiffusion of specific antibodies. A distinct elliptical precipitin arc results for each protein detectable by the antisera.
D007958 Leukocyte Count The number of WHITE BLOOD CELLS per unit volume in venous BLOOD. A differential leukocyte count measures the relative numbers of the different types of white cells. Blood Cell Count, White,Differential Leukocyte Count,Leukocyte Count, Differential,Leukocyte Number,White Blood Cell Count,Count, Differential Leukocyte,Count, Leukocyte,Counts, Differential Leukocyte,Counts, Leukocyte,Differential Leukocyte Counts,Leukocyte Counts,Leukocyte Counts, Differential,Leukocyte Numbers,Number, Leukocyte,Numbers, Leukocyte
D011414 Properdin A 53-kDa protein that is a positive regulator of the alternate pathway of complement activation (COMPLEMENT ACTIVATION PATHWAY, ALTERNATIVE). It stabilizes the ALTERNATIVE PATHWAY C3 CONVERTASE (C3bBb) and protects it from rapid inactivation, thus facilitating the cascade of COMPLEMENT ACTIVATION and the formation of MEMBRANE ATTACK COMPLEX. Individuals with mutation in the PFC gene exhibit properdin deficiency and have a high susceptibility to infections. Complement Factor P,Factor P, Complement
D003095 Collagen Diseases Historically, a heterogeneous group of acute and chronic diseases, including rheumatoid arthritis, systemic lupus erythematosus, progressive systemic sclerosis, dermatomyositis, etc. This classification was based on the notion that "collagen" was equivalent to "connective tissue", but with the present recognition of the different types of collagen and the aggregates derived from them as distinct entities, the term "collagen diseases" now pertains exclusively to those inherited conditions in which the primary defect is at the gene level and affects collagen biosynthesis, post-translational modification, or extracellular processing directly. (From Cecil Textbook of Medicine, 19th ed, p1494) Collagen Disease,Disease, Collagen,Diseases, Collagen
D003165 Complement System Proteins Serum glycoproteins participating in the host defense mechanism of COMPLEMENT ACTIVATION that creates the COMPLEMENT MEMBRANE ATTACK COMPLEX. Included are glycoproteins in the various pathways of complement activation (CLASSICAL COMPLEMENT PATHWAY; ALTERNATIVE COMPLEMENT PATHWAY; and LECTIN COMPLEMENT PATHWAY). Complement Proteins,Complement,Complement Protein,Hemolytic Complement,Complement, Hemolytic,Protein, Complement,Proteins, Complement,Proteins, Complement System
D003176 Complement C3 A glycoprotein that is central in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C3 can be cleaved into COMPLEMENT C3A and COMPLEMENT C3B, spontaneously at low level or by C3 CONVERTASE at high level. The smaller fragment C3a is an ANAPHYLATOXIN and mediator of local inflammatory process. The larger fragment C3b binds with C3 convertase to form C5 convertase. C3 Complement,C3 Precursor,Complement 3,Complement C3 Precursor,Complement Component 3,Precursor-Complement 3,Pro-C3,Pro-Complement 3,C3 Precursor, Complement,C3, Complement,Complement, C3,Component 3, Complement,Precursor Complement 3,Precursor, C3,Precursor, Complement C3,Pro C3,Pro Complement 3
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D001168 Arthritis Acute or chronic inflammation of JOINTS. Oligoarthritis,Polyarthritis,Arthritides,Oligoarthritides,Polyarthritides
D001172 Arthritis, Rheumatoid A chronic systemic disease, primarily of the joints, marked by inflammatory changes in the synovial membranes and articular structures, widespread fibrinoid degeneration of the collagen fibers in mesenchymal tissues, and by atrophy and rarefaction of bony structures. Etiology is unknown, but autoimmune mechanisms have been implicated. Rheumatoid Arthritis
D013582 Synovial Fluid The clear, viscous fluid secreted by the SYNOVIAL MEMBRANE. It contains mucin, albumin, fat, and mineral salts and serves to lubricate joints. Synovia,Fluid, Synovial,Fluids, Synovial,Synovial Fluids

Related Publications

G G Hunder, and F C McDuffie, and B J Mullen
January 1978, Allergie und Immunologie,
G G Hunder, and F C McDuffie, and B J Mullen
January 1991, Zeitschrift fur Rheumatologie,
G G Hunder, and F C McDuffie, and B J Mullen
September 1997, Journal of clinical immunology,
G G Hunder, and F C McDuffie, and B J Mullen
June 2010, Journal of biomedical materials research. Part A,
G G Hunder, and F C McDuffie, and B J Mullen
September 1984, Philosophical transactions of the Royal Society of London. Series B, Biological sciences,
G G Hunder, and F C McDuffie, and B J Mullen
October 1987, Journal of immunology (Baltimore, Md. : 1950),
G G Hunder, and F C McDuffie, and B J Mullen
November 1985, Casopis lekaru ceskych,
G G Hunder, and F C McDuffie, and B J Mullen
January 2000, The Journal of investigative dermatology,
Copied contents to your clipboard!