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Article: Changes and significance of IL-25 in chicken collagen II-induced experimental arthritis (CIA)

TitleChanges and significance of IL-25 in chicken collagen II-induced experimental arthritis (CIA)
Authors
KeywordsCollagen II-induced experimental arthritis (CIA)
IL-25
IL-17
IL-4
DBA/1 mice
Issue Date2012
PublisherSpringer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00296/index.htm
Citation
Rheumatology International: clinical and experimental investigations, 2012, v. 32 n. 8, p. 2331-2338 How to Cite?
AbstractRheumatoid arthritis (RA) is an autoimmune inflammatory disease. It is a systemic inflammatory disease, characterized by chronic, symmetrical, multi-articular synovial arthritis. IL-25 (IL-17E) is a member of the recently emerged cytokine family (IL-17s), which is expressed in Th2 cells and bone marrow-derived mast cells. Unlike the other members of this family, IL-25 is capable of inducing Th2-associated cytokines (IL-4, IL-5, and IL-13) and also promotes the release of some pro-immune factors (IL-6 and IL-8). IL-25 is also a pleiotropic factor, which constitutes a tissue-specific pathological injury and chronic inflammation. In this study, we used chicken collagen II-induced experimental arthritis (CIA) model in DBA/1 mice to investigate the relationship between IL-25 and other inflammatory factors, revealing the possible mechanism in CIA. Our results showed that the expression level of IL-25 was enhanced in the late stage of CIA, and IL-17 was increased in the early stage of the disease. It is well known that IL-17 has a crucial role in the development of RA pathogenesis, and IL-25 plays a significant role in humoral immune. For reasons given above, we suggested that the IL-25 inhibited IL-17 expression to some extent, while enhancing the production of IL-4. It was confirmed that IL-25 not only regulated the cellular immune, but also involved the humoral immune in rheumatoid arthritis.
Persistent Identifierhttp://hdl.handle.net/10722/164851
ISSN
2017 Impact Factor: 1.952
2015 SCImago Journal Rankings: 0.638
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWang, K-
dc.contributor.authorSu, Z-
dc.contributor.authorZhao, Y-
dc.contributor.authorSiamak, SS-
dc.contributor.authorJiao, Z-
dc.contributor.authorXue, Y-
dc.contributor.authorYang, H-
dc.contributor.authorZheng, D-
dc.contributor.authorLiu, Y-
dc.contributor.authorShen, P-
dc.contributor.authorWang, S-
dc.contributor.authorShao, Q-
dc.contributor.authorHuang, X-
dc.contributor.authorLu, L-
dc.contributor.authorXu, H-
dc.date.accessioned2012-09-20T08:10:59Z-
dc.date.available2012-09-20T08:10:59Z-
dc.date.issued2012-
dc.identifier.citationRheumatology International: clinical and experimental investigations, 2012, v. 32 n. 8, p. 2331-2338-
dc.identifier.issn0172-8172-
dc.identifier.urihttp://hdl.handle.net/10722/164851-
dc.description.abstractRheumatoid arthritis (RA) is an autoimmune inflammatory disease. It is a systemic inflammatory disease, characterized by chronic, symmetrical, multi-articular synovial arthritis. IL-25 (IL-17E) is a member of the recently emerged cytokine family (IL-17s), which is expressed in Th2 cells and bone marrow-derived mast cells. Unlike the other members of this family, IL-25 is capable of inducing Th2-associated cytokines (IL-4, IL-5, and IL-13) and also promotes the release of some pro-immune factors (IL-6 and IL-8). IL-25 is also a pleiotropic factor, which constitutes a tissue-specific pathological injury and chronic inflammation. In this study, we used chicken collagen II-induced experimental arthritis (CIA) model in DBA/1 mice to investigate the relationship between IL-25 and other inflammatory factors, revealing the possible mechanism in CIA. Our results showed that the expression level of IL-25 was enhanced in the late stage of CIA, and IL-17 was increased in the early stage of the disease. It is well known that IL-17 has a crucial role in the development of RA pathogenesis, and IL-25 plays a significant role in humoral immune. For reasons given above, we suggested that the IL-25 inhibited IL-17 expression to some extent, while enhancing the production of IL-4. It was confirmed that IL-25 not only regulated the cellular immune, but also involved the humoral immune in rheumatoid arthritis.-
dc.languageeng-
dc.publisherSpringer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00296/index.htm-
dc.relation.ispartofRheumatology International: clinical and experimental investigations-
dc.rightsThe final publication is available at Springer via http://dx.doi.org/[insert DOI]-
dc.subjectCollagen II-induced experimental arthritis (CIA)-
dc.subjectIL-25-
dc.subjectIL-17-
dc.subjectIL-4-
dc.subjectDBA/1 mice-
dc.titleChanges and significance of IL-25 in chicken collagen II-induced experimental arthritis (CIA)-
dc.typeArticle-
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1437-160X (Electronic) 0172-8172 (Linkin&volume=32&issue=8&spage=2331&epage=8&date=2012&atitle=Changes+and+significance+of+IL-25+in+chicken+collagen+II-induced+experimental+arthritis+(CIA)en_US
dc.identifier.emailLu, L: liweilu@hkucc.hku.hk-
dc.identifier.authorityLu, L=rp00477-
dc.identifier.doi10.1007/s00296-011-1955-2-
dc.identifier.pmid21626028-
dc.identifier.scopuseid_2-s2.0-84866259048-
dc.identifier.hkuros208190-
dc.identifier.volume32-
dc.identifier.issue8-
dc.identifier.spage2331-
dc.identifier.epage2338-
dc.identifier.isiWOS:000306827500017-
dc.publisher.placeGermany-
dc.identifier.citeulike9436658-

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