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Article: CD5-positive and CD5-negative rheumatoid factor-secreting B cells in IgA nephropathy, rheumatoid arthritis and Graves' disease

TitleCD5-positive and CD5-negative rheumatoid factor-secreting B cells in IgA nephropathy, rheumatoid arthritis and Graves' disease
Authors
Issue Date1993
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/SJI
Citation
Scandinavian Journal Of Immunology, 1993, v. 38 n. 6, p. 575-580 How to Cite?
AbstractThe relative contributions of CD5+ and CD5- B-cells in production of rheumatoid factors (RF) was evaluated in polyclonally activated B-cells from patients with IgA nephropathy (IgAN), rheumatoid arthritis (RA) and Graves' disease (GD). In IgAN and RA, diseases in which RFs are believed to be involved in pathogenesis, there were 10- and 4-fold decreases respectively in CD5+ IgG-RF-secreting B-cells compared with controls. Furthermore, the number of CD5- IgG-RF- and IgA-RF-secreting B-cells were increased 12- and 14-fold in IgAN and 9- and 4-fold in RA. Such abnormalities were not apparent in GD, in which RFs have not been implicated in pathogenesis. These findings are compatible with the concept of CD5+ RF-secreting B-cells normally acting to prevent production of potentially pathogenic RFs by CD5- B-cells. When IgAN or RA patients' B-cells were activated in the presence of control instead of autologous CD4+ cells, numbers of RF- secreting CD5- B-cells were reduced to the levels seen with control B-cells plus control T-helper cells. Presumably lymphokine secretion profiles of T-helper cells would be important in determining whether CD5+ or CD5- B-cells are activated to secrete RFs, and perhaps therapeutic manipulation of these profiles could restore normal activity of CD5+ B-cells in IgAN and RA.
Persistent Identifierhttp://hdl.handle.net/10722/161961
ISSN
2015 Impact Factor: 2.27
2015 SCImago Journal Rankings: 0.934
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorJones, BMen_US
dc.contributor.authorCheng, IKPen_US
dc.contributor.authorWong, RWSen_US
dc.contributor.authorKung, AWCen_US
dc.date.accessioned2012-09-05T05:16:19Z-
dc.date.available2012-09-05T05:16:19Z-
dc.date.issued1993en_US
dc.identifier.citationScandinavian Journal Of Immunology, 1993, v. 38 n. 6, p. 575-580en_US
dc.identifier.issn0300-9475en_US
dc.identifier.urihttp://hdl.handle.net/10722/161961-
dc.description.abstractThe relative contributions of CD5+ and CD5- B-cells in production of rheumatoid factors (RF) was evaluated in polyclonally activated B-cells from patients with IgA nephropathy (IgAN), rheumatoid arthritis (RA) and Graves' disease (GD). In IgAN and RA, diseases in which RFs are believed to be involved in pathogenesis, there were 10- and 4-fold decreases respectively in CD5+ IgG-RF-secreting B-cells compared with controls. Furthermore, the number of CD5- IgG-RF- and IgA-RF-secreting B-cells were increased 12- and 14-fold in IgAN and 9- and 4-fold in RA. Such abnormalities were not apparent in GD, in which RFs have not been implicated in pathogenesis. These findings are compatible with the concept of CD5+ RF-secreting B-cells normally acting to prevent production of potentially pathogenic RFs by CD5- B-cells. When IgAN or RA patients' B-cells were activated in the presence of control instead of autologous CD4+ cells, numbers of RF- secreting CD5- B-cells were reduced to the levels seen with control B-cells plus control T-helper cells. Presumably lymphokine secretion profiles of T-helper cells would be important in determining whether CD5+ or CD5- B-cells are activated to secrete RFs, and perhaps therapeutic manipulation of these profiles could restore normal activity of CD5+ B-cells in IgAN and RA.en_US
dc.languageengen_US
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/SJIen_US
dc.relation.ispartofScandinavian Journal of Immunologyen_US
dc.subject.meshAdolescenten_US
dc.subject.meshAdulten_US
dc.subject.meshAgeden_US
dc.subject.meshAntigens, Cd - Biosynthesisen_US
dc.subject.meshAntigens, Cd5en_US
dc.subject.meshArthritis, Rheumatoid - Immunologyen_US
dc.subject.meshB-Lymphocyte Subsets - Immunologyen_US
dc.subject.meshB-Lymphocytes - Immunologyen_US
dc.subject.meshChilden_US
dc.subject.meshFemaleen_US
dc.subject.meshGlomerulonephritis, Iga - Immunologyen_US
dc.subject.meshGraves Disease - Immunologyen_US
dc.subject.meshHumansen_US
dc.subject.meshLeukocyte Counten_US
dc.subject.meshLymphocyte Activationen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshRheumatoid Factor - Biosynthesisen_US
dc.titleCD5-positive and CD5-negative rheumatoid factor-secreting B cells in IgA nephropathy, rheumatoid arthritis and Graves' diseaseen_US
dc.typeArticleen_US
dc.identifier.emailKung, AWC:awckung@hku.hken_US
dc.identifier.authorityKung, AWC=rp00368en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1111/j.1365-3083.1993.tb03244.xen_US
dc.identifier.pmid7504827-
dc.identifier.scopuseid_2-s2.0-0027133527en_US
dc.identifier.volume38en_US
dc.identifier.issue6en_US
dc.identifier.spage575en_US
dc.identifier.epage580en_US
dc.identifier.isiWOS:A1993MK36500013-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridJones, BM=7404958958en_US
dc.identifier.scopusauthoridCheng, IKP=7102537483en_US
dc.identifier.scopusauthoridWong, RWS=34875928200en_US
dc.identifier.scopusauthoridKung, AWC=7102322339en_US

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