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Article: Serum levels of IL-33 and soluble ST2 and their association with disease activity in systemic lupus erythematosus

TitleSerum levels of IL-33 and soluble ST2 and their association with disease activity in systemic lupus erythematosus
Authors
KeywordsInterleukin-33
Soluble ST2
Systemic lupus erythematosus disease activity index
T helper 2 immune response
Issue Date2009
PublisherOxford University Press. The Journal's web site is located at http://rheumatology.oxfordjournals.org/
Citation
Rheumatology, 2009, v. 49 n. 3, p. 520-527 How to Cite?
Abstract
Objective. IL-33 has recently been found to be the specific ligand of ST2, an IL-1 receptor family member that is selectively expressed in Th2 cells and mediates Th2 response. This study aims to measure the serum levels of soluble ST2 (sST2) and IL-33 in patients with SLE and to examine their association with disease activity. Methods. Seventy SLE patients were evaluated for disease activity, determined by SLEDAI, levels of anti-dsDNA antibody, C3 and C4. Fifty-seven patients were evaluated longitudinally on a second occasion. IL-33 and sST2 were measured by sandwich ELISA in the 127 SLE serum samples and compared with 28 age-and sex-matched healthy controls. Results. Serum sST2 level was significantly higher in active SLE patients [0.51 (0.18) ng/ml] compared with inactive patients [0.42 (0.08) ng/ml] (P = 0.006) and normal controls [0.36 (0.13) ng/ml] (P<0.001). sST2 level correlated significantly with SLEDAI, anti-dsDNA antibody and prednisolone dosage, and negatively with C3. Linear regression analysis showed that serum sST2 level was an independent predictive factor for modified SLEDAI, excluding anti-dsDNA and complement score after controlling for age, sex, glomerular filtration rate and prednisolone dosage (regression coefficient: 8.5; 95% CI 2.6, 14.3) (P = 0.005). Serum sST2 level was sensitive to change in disease activity longitudinally, with an effect size of 0.29. Elevated serum IL-33 was comparable in frequency (4.3 vs 7.1%; P = 0.62) and levels (P = 0.53) between SLE patients and controls. Conclusions. Elevated serum sST2 level in SLE patients was found to correlate with disease activity and was sensitive to change, suggesting a potential role as a surrogate marker of disease activity. © The Author 2009. Published by Oxford University Press on behalf of the British Society for Rheumatology.
Persistent Identifierhttp://hdl.handle.net/10722/163300
ISSN
2013 Impact Factor: 4.435
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMok, MYen_HK
dc.contributor.authorHuang, FPen_HK
dc.contributor.authorIp, WKen_HK
dc.contributor.authorLo, Yen_HK
dc.contributor.authorWong, FYen_HK
dc.contributor.authorChan, EYTen_HK
dc.contributor.authorLam, KFen_HK
dc.contributor.authorXu, Den_HK
dc.date.accessioned2012-09-05T05:29:50Z-
dc.date.available2012-09-05T05:29:50Z-
dc.date.issued2009en_HK
dc.identifier.citationRheumatology, 2009, v. 49 n. 3, p. 520-527en_HK
dc.identifier.issn1462-0324en_HK
dc.identifier.urihttp://hdl.handle.net/10722/163300-
dc.description.abstractObjective. IL-33 has recently been found to be the specific ligand of ST2, an IL-1 receptor family member that is selectively expressed in Th2 cells and mediates Th2 response. This study aims to measure the serum levels of soluble ST2 (sST2) and IL-33 in patients with SLE and to examine their association with disease activity. Methods. Seventy SLE patients were evaluated for disease activity, determined by SLEDAI, levels of anti-dsDNA antibody, C3 and C4. Fifty-seven patients were evaluated longitudinally on a second occasion. IL-33 and sST2 were measured by sandwich ELISA in the 127 SLE serum samples and compared with 28 age-and sex-matched healthy controls. Results. Serum sST2 level was significantly higher in active SLE patients [0.51 (0.18) ng/ml] compared with inactive patients [0.42 (0.08) ng/ml] (P = 0.006) and normal controls [0.36 (0.13) ng/ml] (P<0.001). sST2 level correlated significantly with SLEDAI, anti-dsDNA antibody and prednisolone dosage, and negatively with C3. Linear regression analysis showed that serum sST2 level was an independent predictive factor for modified SLEDAI, excluding anti-dsDNA and complement score after controlling for age, sex, glomerular filtration rate and prednisolone dosage (regression coefficient: 8.5; 95% CI 2.6, 14.3) (P = 0.005). Serum sST2 level was sensitive to change in disease activity longitudinally, with an effect size of 0.29. Elevated serum IL-33 was comparable in frequency (4.3 vs 7.1%; P = 0.62) and levels (P = 0.53) between SLE patients and controls. Conclusions. Elevated serum sST2 level in SLE patients was found to correlate with disease activity and was sensitive to change, suggesting a potential role as a surrogate marker of disease activity. © The Author 2009. Published by Oxford University Press on behalf of the British Society for Rheumatology.en_HK
dc.languageengen_US
dc.publisherOxford University Press. The Journal's web site is located at http://rheumatology.oxfordjournals.org/en_HK
dc.relation.ispartofRheumatologyen_HK
dc.subjectInterleukin-33en_HK
dc.subjectSoluble ST2en_HK
dc.subjectSystemic lupus erythematosus disease activity indexen_HK
dc.subjectT helper 2 immune responseen_HK
dc.subject.meshAdulten_US
dc.subject.meshAntibodies, Antinuclear - Blooden_US
dc.subject.meshBiological Markers - Blooden_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshEpidemiologic Methodsen_US
dc.subject.meshFemaleen_US
dc.subject.meshGlucocorticoids - Administration & Dosageen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunosuppressive Agents - Administration & Dosageen_US
dc.subject.meshInterleukins - Blooden_US
dc.subject.meshLupus Erythematosus, Systemic - Drug Therapy - Immunologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshPrednisolone - Administration & Dosageen_US
dc.subject.meshReceptors, Cell Surface - Blooden_US
dc.titleSerum levels of IL-33 and soluble ST2 and their association with disease activity in systemic lupus erythematosusen_HK
dc.typeArticleen_HK
dc.identifier.emailMok, MY: temy@hkucc.hku.hken_HK
dc.identifier.emailLam, KF: hrntlkf@hkucc.hku.hken_HK
dc.identifier.authorityMok, MY=rp00490en_HK
dc.identifier.authorityLam, KF=rp00718en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1093/rheumatology/kep402en_HK
dc.identifier.pmid20026564en_HK
dc.identifier.scopuseid_2-s2.0-77950534152en_HK
dc.identifier.hkuros234991-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77950534152&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume49en_HK
dc.identifier.issue3en_HK
dc.identifier.spage520en_HK
dc.identifier.epage527en_HK
dc.identifier.isiWOS:000274487000016-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridMok, MY=7006024184en_HK
dc.identifier.scopusauthoridHuang, FP=55238926300en_HK
dc.identifier.scopusauthoridIp, WK=36999273200en_HK
dc.identifier.scopusauthoridLo, Y=35148230000en_HK
dc.identifier.scopusauthoridWong, FY=36999602700en_HK
dc.identifier.scopusauthoridChan, EYT=7401994013en_HK
dc.identifier.scopusauthoridLam, KF=8948421200en_HK
dc.identifier.scopusauthoridXu, D=7404073685en_HK

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