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Article: A proinflammatory role of IL-18 in the development of spontaneous autoimmune disease

TitleA proinflammatory role of IL-18 in the development of spontaneous autoimmune disease
Authors
Issue Date2001
PublisherAmerican Association of Immunologists. The Journal's web site is located at http://www.jimmunol.org
Citation
Journal of Immunology, 2001, v. 167 n. 9, p. 5338-5347 How to Cite?
AbstractSerum from patients with systemic lupus erythematosus (SLE) contained significantly higher concentrations of IL-18 than normal individuals. MRL/lpr mice, which develop spontaneous lupus-like autoimmune disease, also had higher serum levels of IL-18 than wild-type MRL/++ mice. Daily injections of IL-18 or IL-18 plus IL-12 resulted in accelerated proteinuria, glomerulonephritis, vasculitis, and raised levels of proinflammatory cytokines in MRL/lpr mice. IL-18-treated MRL/lpr mice also developed a 'butterfly' facial rash resembling clinical SLE. In contrast, MRL/lpr mice treated with IL-18 plus IL-12 did not develop a facial rash. The facial lesion in the IL-18-treated mice showed epidermal thickening with intense chronic inflammation accompanied by increased apoptosis, Ig deposition, and early systemic Th2 response compared with control or IL-12 plus IL-18-treated mice. These data therefore show that IL-18 is an important mediator of lupus-like disease and may thus be a novel target for therapeutic intervention of spontaneous autoimmune diseases.
Persistent Identifierhttp://hdl.handle.net/10722/49419
ISSN
2015 Impact Factor: 4.985
2015 SCImago Journal Rankings: 3.549
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorEsfandiari, Een_HK
dc.contributor.authorMcInnes, IBen_HK
dc.contributor.authorLindop, Gen_HK
dc.contributor.authorHuang, FPen_HK
dc.contributor.authorField, Men_HK
dc.contributor.authorKomai-Koma, Men_HK
dc.contributor.authorWei, XQen_HK
dc.contributor.authorLiew, FYen_HK
dc.date.accessioned2008-06-12T06:42:05Z-
dc.date.available2008-06-12T06:42:05Z-
dc.date.issued2001en_HK
dc.identifier.citationJournal of Immunology, 2001, v. 167 n. 9, p. 5338-5347en_HK
dc.identifier.issn0022-1767en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49419-
dc.description.abstractSerum from patients with systemic lupus erythematosus (SLE) contained significantly higher concentrations of IL-18 than normal individuals. MRL/lpr mice, which develop spontaneous lupus-like autoimmune disease, also had higher serum levels of IL-18 than wild-type MRL/++ mice. Daily injections of IL-18 or IL-18 plus IL-12 resulted in accelerated proteinuria, glomerulonephritis, vasculitis, and raised levels of proinflammatory cytokines in MRL/lpr mice. IL-18-treated MRL/lpr mice also developed a 'butterfly' facial rash resembling clinical SLE. In contrast, MRL/lpr mice treated with IL-18 plus IL-12 did not develop a facial rash. The facial lesion in the IL-18-treated mice showed epidermal thickening with intense chronic inflammation accompanied by increased apoptosis, Ig deposition, and early systemic Th2 response compared with control or IL-12 plus IL-18-treated mice. These data therefore show that IL-18 is an important mediator of lupus-like disease and may thus be a novel target for therapeutic intervention of spontaneous autoimmune diseases.en_HK
dc.format.extent420 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherAmerican Association of Immunologists. The Journal's web site is located at http://www.jimmunol.orgen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsThis is an author-produced version of a manuscript accepted for publication in The Journal of Immunology (The JI). The American Association of Immunologists, Inc. (The AAI), publisher of The JI, holds the copyright to this manuscript. This manuscript has not yet been copyedited or subjected to editorial proofreading by The JI; hence, it may differ from the final version published in The JI (online and in print). The AAI (The JI) is not liable for errors or omissions in this author-produced version of the manuscript or in any version derived from it by the National Institutes of Health or any other third party. The final, citable version of record can be found at www.jimmunol.orgen_HK
dc.subject.meshAutoimmune Diseases - etiology - pathology - therapyen_HK
dc.subject.meshInterleukin-18 - physiologyen_HK
dc.subject.meshAntibodies, Antinuclear - blooden_HK
dc.subject.meshCytokines - biosynthesisen_HK
dc.subject.meshInterleukin-12 - pharmacologyen_HK
dc.titleA proinflammatory role of IL-18 in the development of spontaneous autoimmune diseaseen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-1767&volume=167&issue=9&spage=5338&epage=5347&date=2001&atitle=A+proinflammatory+role+of+IL-18+in+the+development+of+spontaneous+autoimmune+diseaseen_HK
dc.identifier.emailHuang, FP: fphuang@hkucc.hku.hken_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.pmid11673550en_HK
dc.identifier.scopuseid_2-s2.0-0035500546-
dc.identifier.hkuros66009-
dc.identifier.isiWOS:000171858500071-

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