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Article: CD4-positive cells from patients with IgA nephropathy demonstrate increased mRNA of cytokines that induce the IgA switch and differentiation

TitleCD4-positive cells from patients with IgA nephropathy demonstrate increased mRNA of cytokines that induce the IgA switch and differentiation
Authors
KeywordsCytokine
IgA nephropathy
IgA synthesis
Interleukin 5
mRNA
Transforming growth factor-β
Issue Date1994
PublisherJohn Wiley & Sons. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/1130
Citation
Journal Of Pathology, 1994, v. 174 n. 1, p. 13-22 How to Cite?
AbstractIgA nephropathy (IgAN) is characterized by raised serum IgA1 and mesangial IgA1 deposits. We have previously shown increased T-cell activation in IgAN. Recently, transforming growth factor-β (TGF-β) has been shown to induce IgA isotype switch at a clonal level and interleukin 5 (IL5) promotes differentiation into IgA-bearing B cells. In the present study we have examined the TGF-β and IL5 mRNA expression by mitogen-activated CD4-positive T cells from patients with IgAN (n = 25), patients with other primary nephritides (CGN) (n = 24), and healthy control subjects (n = 25). The cytokine genes were analysed by reverse transcription (RT)-polymerase chain reaction (PCR) and were semi-quantitated by normalizing the differences occurring during RT and PCR using a housekeeping gene, β-actin. CDC-positive T cells from IgA nephritic patients expressed a higher level of IL5 mRNA than healthy controls (P < 0.01) and patients with CGN (P < 0.005). CD4-positive T cells from IgA nephritic patients expressed a higher level of TGF-β mRNA than healthy controls (P < 0.01) but no difference was demonstrated on comparison with CGN patients. Elevated TGF-β mRNA expression in patients with CGN probably reflects its other important function as a 'sclerogenic' factor involved in the glomerulosclerosis found in these nephritides. Our data suggest that there is increased expression of cytokine genes which induce the IgA isotype switch and differentiation; these immunological abnormalities may be important in the pathogenesis of IgAN.
Persistent Identifierhttp://hdl.handle.net/10722/162028
ISSN
2015 Impact Factor: 7.381
2015 SCImago Journal Rankings: 4.176
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLai, KNen_HK
dc.contributor.authorHo, RTHen_HK
dc.contributor.authorLeung, JCKen_HK
dc.contributor.authorChui, YLen_HK
dc.contributor.authorLim, PLen_HK
dc.contributor.authorLui, SFen_HK
dc.contributor.authorLi, PKTen_HK
dc.date.accessioned2012-09-05T05:16:45Z-
dc.date.available2012-09-05T05:16:45Z-
dc.date.issued1994en_HK
dc.identifier.citationJournal Of Pathology, 1994, v. 174 n. 1, p. 13-22en_HK
dc.identifier.issn0022-3417en_HK
dc.identifier.urihttp://hdl.handle.net/10722/162028-
dc.description.abstractIgA nephropathy (IgAN) is characterized by raised serum IgA1 and mesangial IgA1 deposits. We have previously shown increased T-cell activation in IgAN. Recently, transforming growth factor-β (TGF-β) has been shown to induce IgA isotype switch at a clonal level and interleukin 5 (IL5) promotes differentiation into IgA-bearing B cells. In the present study we have examined the TGF-β and IL5 mRNA expression by mitogen-activated CD4-positive T cells from patients with IgAN (n = 25), patients with other primary nephritides (CGN) (n = 24), and healthy control subjects (n = 25). The cytokine genes were analysed by reverse transcription (RT)-polymerase chain reaction (PCR) and were semi-quantitated by normalizing the differences occurring during RT and PCR using a housekeeping gene, β-actin. CDC-positive T cells from IgA nephritic patients expressed a higher level of IL5 mRNA than healthy controls (P < 0.01) and patients with CGN (P < 0.005). CD4-positive T cells from IgA nephritic patients expressed a higher level of TGF-β mRNA than healthy controls (P < 0.01) but no difference was demonstrated on comparison with CGN patients. Elevated TGF-β mRNA expression in patients with CGN probably reflects its other important function as a 'sclerogenic' factor involved in the glomerulosclerosis found in these nephritides. Our data suggest that there is increased expression of cytokine genes which induce the IgA isotype switch and differentiation; these immunological abnormalities may be important in the pathogenesis of IgAN.en_HK
dc.languageengen_US
dc.publisherJohn Wiley & Sons. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/1130en_HK
dc.relation.ispartofJournal of Pathologyen_HK
dc.subjectCytokineen_HK
dc.subjectIgA nephropathyen_HK
dc.subjectIgA synthesisen_HK
dc.subjectInterleukin 5en_HK
dc.subjectmRNAen_HK
dc.subjectTransforming growth factor-βen_HK
dc.subject.meshAdulten_US
dc.subject.meshBase Sequenceen_US
dc.subject.meshCd4-Positive T-Lymphocytes - Immunologyen_US
dc.subject.meshCytokines - Geneticsen_US
dc.subject.meshFemaleen_US
dc.subject.meshGene Expressionen_US
dc.subject.meshGlomerulonephritis, Iga - Genetics - Immunologyen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunoglobulin A - Biosynthesis - Blooden_US
dc.subject.meshInterleukin-5 - Geneticsen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshMolecular Sequence Dataen_US
dc.subject.meshPolymerase Chain Reaction - Methodsen_US
dc.subject.meshRna, Messenger - Geneticsen_US
dc.subject.meshTransforming Growth Factor Beta - Geneticsen_US
dc.titleCD4-positive cells from patients with IgA nephropathy demonstrate increased mRNA of cytokines that induce the IgA switch and differentiationen_HK
dc.typeArticleen_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.emailHo, RTH: tinho@hku.hken_HK
dc.identifier.emailLeung, JCK: jckleung@hku.hken_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.identifier.authorityHo, RTH=rp00497en_HK
dc.identifier.authorityLeung, JCK=rp00448en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/path.1711740104en_HK
dc.identifier.pmid7965399-
dc.identifier.scopuseid_2-s2.0-0028019688en_HK
dc.identifier.volume174en_HK
dc.identifier.issue1en_HK
dc.identifier.spage13en_HK
dc.identifier.epage22en_HK
dc.identifier.isiWOS:A1994PM10600003-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK
dc.identifier.scopusauthoridHo, RTH=8620896500en_HK
dc.identifier.scopusauthoridLeung, JCK=7202180349en_HK
dc.identifier.scopusauthoridChui, YL=7004982375en_HK
dc.identifier.scopusauthoridLim, PL=7202592401en_HK
dc.identifier.scopusauthoridLui, SF=7102379144en_HK
dc.identifier.scopusauthoridLi, PKT=25928016800en_HK

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