Biomaterial Database

Complement-mediated solubilization of immune complexes. Solubilization inhibition and complement factor levels in SLE patients. 1984

G Baatrup, and I Petersen, and E Kappelgaard, and H H Jepsen, and S E Svehag

Thirty-two of 36 serum samples from 19 SLE patients showed reduced capacity to mediate complement-dependent solubilization of immune complexes (IC). SLE patients with nephritis exerted the lowest complement-mediated solubilization capacity (CMSC) whereas sera from patients with inactive disease gave the highest CMSC values, with three out of four samples within the normal reference range. Thirty-five of the 36 serum samples showed inhibition of CMSC in a newly developed CMSC inhibition assay. The strongest CMSC inhibition was exerted by sera from newly discovered cases of SLE who received no medical treatment and the lowest inhibition by sera from patients with inactive disease. There was a significant negative correlation between CMSC and CMSC inhibition (r = -0.67, P less than 0.001). Sera with low concentrations of C1q, C3, factor B or high C3d levels showed markedly reduced CMSC values. Pronounced CMSC inhibition was observed only in samples with normal or high factor H values. No significant correlation was found between CMSC or CMSC inhibition and circulating IC levels, but pronounced CMSC inhibition was registered only in strongly IC positive sera.

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
D008297	Male		Males
D008875	Middle Aged	An adult aged 45 - 64 years.	Middle Age
D010956	Plasmapheresis	Procedure whereby plasma is separated and extracted from anticoagulated whole blood and the red cells retransfused to the donor. Plasmapheresis is also employed for therapeutic use.	Double Filtration Plasmapheresis,Therapeutic Immunoadsorption,Therapeutic Plasma Adsorption,Therapeutic Plasmapheresis,Adsorption, Therapeutic Plasma,Adsorptions, Therapeutic Plasma,Double Filtration Plasmaphereses,Filtration Plasmapheresis, Double,Immunoadsorption, Therapeutic,Plasma Adsorption, Therapeutic,Plasmaphereses,Plasmapheresis, Double Filtration,Plasmapheresis, Therapeutic,Therapeutic Immunoadsorptions,Therapeutic Plasma Adsorptions,Therapeutic Plasmaphereses
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
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
D003166	Complement Activating Enzymes	Enzymes that activate one or more COMPLEMENT PROTEINS in the complement system leading to the formation of the COMPLEMENT MEMBRANE ATTACK COMPLEX, an important response in host defense. They are enzymes in the various COMPLEMENT ACTIVATION pathways.	Activating Enzymes, Complement,Enzymes, Complement Activating
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
D003180	Complement C3b Inactivator Proteins	Endogenous proteins that inhibit or inactivate COMPLEMENT C3B. They include COMPLEMENT FACTOR H and COMPLEMENT FACTOR I (C3b/C4b inactivator). They cleave or promote the cleavage of C3b into inactive fragments, and thus are important in the down-regulation of COMPLEMENT ACTIVATION and its cytolytic sequence.	C3b Inactivators,C3b Inhibitors,Complement 3b Inactivators,Complement 3b Inhibitors,Complement C3b Inactivators,Complement C3b Inhibitor Proteins,Conglutinogen Activating Factors,Factors, Conglutinogen Activating,Inactivators, C3b,Inactivators, Complement 3b,Inactivators, Complement C3b,Inhibitors, C3b,Inhibitors, Complement 3b
D005260	Female		Females