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Titolo:
Autoantibodies to GPI in rheumatoid arthritis: linkage between an animal model and human disease
Autore:
Schaller, M; Burton, DR; Ditzel, HJ;
Indirizzi:
Scripps Clin, Res Inst, Dept Immunol, IMM2, La Jolla, CA 92037 USA ScrippsClin La Jolla CA USA 92037 Immunol, IMM2, La Jolla, CA 92037 USA Scripps Clin, Res Inst, Dept Mol Biol, IMM2, La Jolla, CA 92037 USA Scripps Clin La Jolla CA USA 92037 Mol Biol, IMM2, La Jolla, CA 92037 USA
Titolo Testata:
NATURE IMMUNOLOGY
fascicolo: 8, volume: 2, anno: 2001,
pagine: 746 - 753
SICI:
1529-2908(200108)2:8<746:ATGIRA>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
AUTOCRINE MOTILITY FACTOR; ENDOTHELIAL GROWTH-FACTOR; REACTIVE B-CELLS; T-CELL; PHOSPHOHEXOSE ISOMERASE; MONOCLONAL-ANTIBODY; NEUROTROPHIC FACTOR; AUTOIMMUNE-DISEASE; MOLECULAR-CLONING; NEUROLEUKIN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Ditzel, HJ Scripps Clin, Res Inst, Dept Immunol, IMM2, 10666 N Torrey Pines Rd, La Jolla, CA 92037 USA Scripps Clin 10666 N Torrey Pines Rd La Jolla CA USA 92037 USA
Citazione:
M. Schaller et al., "Autoantibodies to GPI in rheumatoid arthritis: linkage between an animal model and human disease", NAT IMMUNOL, 2(8), 2001, pp. 746-753

Abstract

In K/BxN T cell receptor-transgenic mice, spontaneous inflammatory arthritis exhibiting many of the features of human rheumatoid arthritis (RA) is initiated by T cells, but is almost entirely sustained by antibodies to the self-antigen glucose-6-phosphate isomerase (GPI). The relevance of these observations to human disease has been questioned. Here we show that 64% of humans with RA, but not controls, had increased concentrations of anti-GPI immunoglobulin G (IgG) in serum and synovial fluid. In addition, the concentrations of soluble GPI in the sera and synovial fluids of RA patients were also elevated, which led to immune complex formation. Using phage-display methods, we cloned a panel of specific high-affinity human monoclonal anti-GPI IgGs from a patient with RA. These antibodies were highly somatically mutated, which was indicative of an affinity-matured response that was antigendriven. Immunohistochemistry of RA synovium showed high concentrations of GPI on the surface of the synovial lining and on the endothelial cell surface of arterioles; this indicated a mechanism by which antibodies to GPI mayprecipitate joint disease. The results indicate that the immunological events that lead to the development of autoimmune disease in the K/BxN mouse model may also occur in human RA. This data may be used to develop new strategies for therapeutic intervention.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/03/20 alle ore 22:45:05