Cell-bound complement biomarkers for systemic lupus erythematosus: from benchtop to bedside. 2010

Chau-Ching Liu, and Susan Manzi, and Amy H Kao, and Jeannine S Navratil, and Joseph M Ahearn
Lupus Center of Excellence, University of Pittsburgh School of Health Sciences, Pittsburgh, PA 15260, USA.

Systemic lupus erythematosus is arguably the most clinically and serologically diverse autoimmune disease. This article highlights the biomarkers helpful in diagnosing this disease. The authors' own research is presented.

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
D010446 Peptide Fragments Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques. Peptide Fragment,Fragment, Peptide,Fragments, Peptide
D010641 Phenotype The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment. Phenotypes
D001773 Blood Cells The cells found in the body fluid circulating throughout the CARDIOVASCULAR SYSTEM. Blood Corpuscles,Blood Cell,Blood Corpuscle,Cell, Blood,Cells, Blood,Corpuscle, Blood,Corpuscles, Blood
D003167 Complement Activation The sequential activation of serum COMPLEMENT PROTEINS to create the COMPLEMENT MEMBRANE ATTACK COMPLEX. Factors initiating complement activation include ANTIGEN-ANTIBODY COMPLEXES, microbial ANTIGENS, or cell surface POLYSACCHARIDES. Activation, Complement,Activations, Complement,Complement Activations
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D015415 Biomarkers Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, ENVIRONMENTAL EXPOSURE and its effects, disease diagnosis; METABOLIC PROCESSES; SUBSTANCE ABUSE; PREGNANCY; cell line development; EPIDEMIOLOGIC STUDIES; etc. Biochemical Markers,Biological Markers,Biomarker,Clinical Markers,Immunologic Markers,Laboratory Markers,Markers, Biochemical,Markers, Biological,Markers, Clinical,Markers, Immunologic,Markers, Laboratory,Markers, Serum,Markers, Surrogate,Markers, Viral,Serum Markers,Surrogate Markers,Viral Markers,Biochemical Marker,Biologic Marker,Biologic Markers,Clinical Marker,Immune Marker,Immune Markers,Immunologic Marker,Laboratory Marker,Marker, Biochemical,Marker, Biological,Marker, Clinical,Marker, Immunologic,Marker, Laboratory,Marker, Serum,Marker, Surrogate,Serum Marker,Surrogate End Point,Surrogate End Points,Surrogate Endpoint,Surrogate Endpoints,Surrogate Marker,Viral Marker,Biological Marker,End Point, Surrogate,End Points, Surrogate,Endpoint, Surrogate,Endpoints, Surrogate,Marker, Biologic,Marker, Immune,Marker, Viral,Markers, Biologic,Markers, Immune
D015933 Complement C3d A 302-amino-acid fragment in the alpha chain (672-1663) of C3b. It is generated when C3b is inactivated (iC3b) and its alpha chain is cleaved by COMPLEMENT FACTOR I into C3c, and C3dg (955-1303) in the presence COMPLEMENT FACTOR H. Serum proteases further degrade C3dg into C3d (1002-1303) and C3g (955-1001). C3d Complement,Complement 3d,Complement C3d Fragment,Complement Component 3d,C3d Fragment, Complement,C3d, Complement,Complement, C3d,Component 3d, Complement,Fragment, Complement C3d
D015935 Complement C4b The large fragment formed when COMPLEMENT C4 is cleaved by COMPLEMENT C1S. The membrane-bound C4b binds COMPLEMENT C2A, a SERINE PROTEASE, to form C4b2a (CLASSICAL PATHWAY C3 CONVERTASE) and subsequent C4b2a3b (CLASSICAL PATHWAY C5 CONVERTASE). C4b Complement,Complement 4b,Complement Component 4b,C4b, Complement,Complement, C4b,Component 4b, Complement

Related Publications

Chau-Ching Liu, and Susan Manzi, and Amy H Kao, and Jeannine S Navratil, and Joseph M Ahearn
November 2004, Arthritis and rheumatism,
Chau-Ching Liu, and Susan Manzi, and Amy H Kao, and Jeannine S Navratil, and Joseph M Ahearn
January 2016, Case reports in rheumatology,
Chau-Ching Liu, and Susan Manzi, and Amy H Kao, and Jeannine S Navratil, and Joseph M Ahearn
August 2016, Lupus,
Chau-Ching Liu, and Susan Manzi, and Amy H Kao, and Jeannine S Navratil, and Joseph M Ahearn
October 2012, International journal of rheumatic diseases,
Chau-Ching Liu, and Susan Manzi, and Amy H Kao, and Jeannine S Navratil, and Joseph M Ahearn
December 2012, Arthritis and rheumatism,
Chau-Ching Liu, and Susan Manzi, and Amy H Kao, and Jeannine S Navratil, and Joseph M Ahearn
July 1964, Lancet (London, England),
Chau-Ching Liu, and Susan Manzi, and Amy H Kao, and Jeannine S Navratil, and Joseph M Ahearn
July 2017, Journal of immunological methods,
Chau-Ching Liu, and Susan Manzi, and Amy H Kao, and Jeannine S Navratil, and Joseph M Ahearn
August 2017, Biomarkers in medicine,
Chau-Ching Liu, and Susan Manzi, and Amy H Kao, and Jeannine S Navratil, and Joseph M Ahearn
November 2013, Expert opinion on medical diagnostics,
Chau-Ching Liu, and Susan Manzi, and Amy H Kao, and Jeannine S Navratil, and Joseph M Ahearn
July 1979, Arthritis and rheumatism,
Copied contents to your clipboard!