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Article: T-lymphocyte activation in IgA nephropathy: Serum-soluble interleukin 2 receptor level, interleukin 2 production, and interleukin 2 receptor expression by cultured lymphocytes

TitleT-lymphocyte activation in IgA nephropathy: Serum-soluble interleukin 2 receptor level, interleukin 2 production, and interleukin 2 receptor expression by cultured lymphocytes
Authors
Keywordscellular and soluble interleukin 2 receptor
IgA nephropathy
interleukin 2
lymphocyte
Issue Date1989
PublisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0271-9142
Citation
Journal Of Clinical Immunology, 1989, v. 9 n. 6, p. 485-492 How to Cite?
AbstractThe present study was undertaken to examine the T-lymphocyte activation in IgA nephropathy. Serum-soluble interleukin 2 receptor (sIL2R) levels were studied in 29 IgA nephritic patients, 17 patients with chronic glomerulonephritis (non-IgA nephropathy), and 30 healthy controls during an infection-free period. No difference in serum sIL2R level was demonstrated among these three groups of subjects. However, the serum sIL2R levels of IgA nephritic patient rose significantly during clinical exacerbation with synpharyngitic macroscopic hematuria and the serum sIL2R levels fell when hematuria subsided. Mitogen-stimulated cellular interleukin 2 receptor (IL2R) expression, sIL2R release, and interleukin 2 (IL2) production were also examined in peripheral blood mononuclear cells (PBMC) cultured for 24-48 hr in 21 patients with IgA nephropathy, 17 patients with chronic glomerulo-nephritides, and 17 healthy controls. The total cellular IL2R expression and sIL2R release did not differ among these three groups of subjects. However, the individual T-cell subsets bearing IL2R were distinctly different between IgA nephritic patients and the other two groups of controls. IgA nephritic patients had increased activated CD4+ lymphocytes and reduced activated CD8+ lymphocytes. Furthermore, IL2 production in response to phytohemagglutinin and pokeweed mitogen stimulation was increased in lymphocytes from patients with IgA nephropathy. The IL2 production did not correlate with the quantities of cellular and sIL2R yet the cellular IL2R expression paralleled the sIL2R released by cultured lymphocytes. Our present study suggests that the T lymphocytes from patients with IgA nephropathy have a defect in overproduction of IL2 and increased activated T helper-cell subset upon mitogenic stimulation. Serum measurement of sIL2R could potentially be useful in monitoring the disease activity.
Persistent Identifierhttp://hdl.handle.net/10722/161812
ISSN
2015 Impact Factor: 3.094
2015 SCImago Journal Rankings: 1.332
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorNeng Lai, Ken_HK
dc.contributor.authorLeung, JCKen_HK
dc.contributor.authorMacMoune Lai, Fen_HK
dc.contributor.authorTam, JSen_HK
dc.date.accessioned2012-09-05T05:15:14Z-
dc.date.available2012-09-05T05:15:14Z-
dc.date.issued1989en_HK
dc.identifier.citationJournal Of Clinical Immunology, 1989, v. 9 n. 6, p. 485-492en_HK
dc.identifier.issn0271-9142en_HK
dc.identifier.urihttp://hdl.handle.net/10722/161812-
dc.description.abstractThe present study was undertaken to examine the T-lymphocyte activation in IgA nephropathy. Serum-soluble interleukin 2 receptor (sIL2R) levels were studied in 29 IgA nephritic patients, 17 patients with chronic glomerulonephritis (non-IgA nephropathy), and 30 healthy controls during an infection-free period. No difference in serum sIL2R level was demonstrated among these three groups of subjects. However, the serum sIL2R levels of IgA nephritic patient rose significantly during clinical exacerbation with synpharyngitic macroscopic hematuria and the serum sIL2R levels fell when hematuria subsided. Mitogen-stimulated cellular interleukin 2 receptor (IL2R) expression, sIL2R release, and interleukin 2 (IL2) production were also examined in peripheral blood mononuclear cells (PBMC) cultured for 24-48 hr in 21 patients with IgA nephropathy, 17 patients with chronic glomerulo-nephritides, and 17 healthy controls. The total cellular IL2R expression and sIL2R release did not differ among these three groups of subjects. However, the individual T-cell subsets bearing IL2R were distinctly different between IgA nephritic patients and the other two groups of controls. IgA nephritic patients had increased activated CD4+ lymphocytes and reduced activated CD8+ lymphocytes. Furthermore, IL2 production in response to phytohemagglutinin and pokeweed mitogen stimulation was increased in lymphocytes from patients with IgA nephropathy. The IL2 production did not correlate with the quantities of cellular and sIL2R yet the cellular IL2R expression paralleled the sIL2R released by cultured lymphocytes. Our present study suggests that the T lymphocytes from patients with IgA nephropathy have a defect in overproduction of IL2 and increased activated T helper-cell subset upon mitogenic stimulation. Serum measurement of sIL2R could potentially be useful in monitoring the disease activity.en_HK
dc.languageengen_US
dc.publisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0271-9142en_HK
dc.relation.ispartofJournal of Clinical Immunologyen_HK
dc.subjectcellular and soluble interleukin 2 receptoren_HK
dc.subjectIgA nephropathyen_HK
dc.subjectinterleukin 2en_HK
dc.subjectlymphocyteen_HK
dc.subject.meshAdulten_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshFemaleen_US
dc.subject.meshGlomerulonephritis - Immunologyen_US
dc.subject.meshGlomerulonephritis, Iga - Immunologyen_US
dc.subject.meshHumansen_US
dc.subject.meshInterleukin-2 - Biosynthesisen_US
dc.subject.meshLymphocyte Activation - Immunologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMitogens - Pharmacologyen_US
dc.subject.meshRadioimmunoassayen_US
dc.subject.meshReceptors, Interleukin-2 - Biosynthesis - Blooden_US
dc.subject.meshT-Lymphocytes - Immunologyen_US
dc.titleT-lymphocyte activation in IgA nephropathy: Serum-soluble interleukin 2 receptor level, interleukin 2 production, and interleukin 2 receptor expression by cultured lymphocytesen_HK
dc.typeArticleen_HK
dc.identifier.emailNeng Lai, K: knlai@hku.hken_HK
dc.identifier.emailLeung, JCK: jckleung@hku.hken_HK
dc.identifier.authorityNeng Lai, K=rp00324en_HK
dc.identifier.authorityLeung, JCK=rp00448en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1007/BF00918018en_HK
dc.identifier.pmid2630571-
dc.identifier.scopuseid_2-s2.0-0024848209en_HK
dc.identifier.volume9en_HK
dc.identifier.issue6en_HK
dc.identifier.spage485en_HK
dc.identifier.epage492en_HK
dc.identifier.isiWOS:A1989CF74200007-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridNeng Lai, K=7402135706en_HK
dc.identifier.scopusauthoridLeung, JCK=7202180349en_HK
dc.identifier.scopusauthoridMacMoune Lai, F=6701570301en_HK
dc.identifier.scopusauthoridTam, JS=24788939600en_HK

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