Determination of the second component of complement (C2) by electroimmunoassay in sera from patients with systemic lupus erythematosus. 1983

A Ueda, and T Kusaba, and T Yanase

The concentration of C2 was determined by electroimmunoassay in sera from healthy controls, patients with systemic lupus erythematosus (SLE), their relatives and patients with other diseases. Monospecific anti-human C2 serum was obtained by immunizing rabbits with purified human C2 and then absorbing the rabbit serum with inactivated normal human serum that was made insoluble. In addition, it was shown that human C2 could be purified by means of affinity chromatography on anti-C2 antibody coupled Sepharose. The serum concentration of C2 was 37.8 +/- 5.0 (s.d.) micrograms/ml in healthy controls (n = 133). In patients with SLE, the values were below normal in the active phase and were within normal limits in the inactive phase, showing good correlations with other complement parameters such as CH50, C4, C3 and factor B. C2 concentration was well correlated with C2 haemolytic activity in the inactive phase of SLE, but there was no relationship between the two in the active phase. The mean value of C2 concentration in the relatives of patients with SLE showed no significant difference from that in healthy controls. C2 concentration tended to be high in patients with scleroderma, polymyositis, rheumatoid arthritis, Behçet's disease and aortitis syndrome. However, the values were often low in patients with chronic liver diseases, suggesting a decrease of C2 production in the liver.

UI MeSH Term Description Entries
D008180 Lupus Erythematosus, Systemic A chronic, relapsing, inflammatory, and often febrile multisystemic disorder of connective tissue, characterized principally by involvement of the skin, joints, kidneys, and serosal membranes. It is of unknown etiology, but is thought to represent a failure of the regulatory mechanisms of the autoimmune system. The disease is marked by a wide range of system dysfunctions, an elevated erythrocyte sedimentation rate, and the formation of LE cells in the blood or bone marrow. Libman-Sacks Disease,Lupus Erythematosus Disseminatus,Systemic Lupus Erythematosus,Disease, Libman-Sacks,Libman Sacks Disease
D011415 Complement Factor B A glycine-rich, heat-labile serum glycoprotein that contains a component of the C3 CONVERTASE ALTERNATE PATHWAY (C3bBb). Bb, a serine protease, is generated when factor B is cleaved by COMPLEMENT FACTOR D into Ba and Bb. C3 Proactivator,C3PA,Complement 3 Proactivator,Factor B,Properdin Factor B,Bb Fragment of Factor B,Complement Factor B Fragment, Bb,Complement Factor B, Alternative Pathway,Complement Factor B-Derived Fragment Bb,Complement Factor Ba,Complement Factor Bb,Complement Protein B,Complement Protein Factor B,Properdin Factor Ba,Properdin Factor Bb,Properdin Factor Bf,Properdin Factor Bf F1,Bb, Complement Factor,Complement Factor B Derived Fragment Bb,Factor B, Complement,Factor B, Properdin,Factor Ba, Complement,Factor Ba, Properdin,Factor Bb, Complement,Factor Bb, Properdin,Factor Bf, Properdin,Proactivator, C3,Proactivator, Complement 3,Protein B, Complement
D002846 Chromatography, Affinity A chromatographic technique that utilizes the ability of biological molecules, often ANTIBODIES, to bind to certain ligands specifically and reversibly. It is used in protein biochemistry. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed) Chromatography, Bioaffinity,Immunochromatography,Affinity Chromatography,Bioaffinity Chromatography
D003175 Complement C2 A component of the CLASSICAL COMPLEMENT PATHWAY. C2 is cleaved by activated COMPLEMENT C1S into COMPLEMENT C2B and COMPLEMENT C2A. C2a, the COOH-terminal fragment containing a SERINE PROTEASE, combines with COMPLEMENT C4B to form C4b2a (CLASSICAL PATHWAY C3 CONVERTASE) and subsequent C4b2a3b (CLASSICAL PATHWAY C5 CONVERTASE). C2 Complement,Complement 2,Complement Component 2,C2, Complement,Complement, C2,Component 2, Complement
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
D003181 Complement C4 A glycoprotein that is important in the activation of CLASSICAL COMPLEMENT PATHWAY. C4 is cleaved by the activated COMPLEMENT C1S into COMPLEMENT C4A and COMPLEMENT C4B. C4 Complement,C4 Complement Component,Complement 4,Complement C4, Precursor,Complement Component 4,Pro-C4,Pro-complement 4,C4, Complement,Complement Component, C4,Complement, C4,Component 4, Complement,Component, C4 Complement,Pro C4,Pro complement 4
D004591 Electrophoresis, Polyacrylamide Gel Electrophoresis in which a polyacrylamide gel is used as the diffusion medium. Polyacrylamide Gel Electrophoresis,SDS-PAGE,Sodium Dodecyl Sulfate-PAGE,Gel Electrophoresis, Polyacrylamide,SDS PAGE,Sodium Dodecyl Sulfate PAGE,Sodium Dodecyl Sulfate-PAGEs
D005779 Immunodiffusion Technique involving the diffusion of antigen or antibody through a semisolid medium, usually agar or agarose gel, with the result being a precipitin reaction. Gel Diffusion Tests,Diffusion Test, Gel,Diffusion Tests, Gel,Gel Diffusion Test,Immunodiffusions,Test, Gel Diffusion,Tests, Gel Diffusion
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man

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