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Article: Arthritis susceptibility in mice expressing human type II collagen in cartilage

TitleArthritis susceptibility in mice expressing human type II collagen in cartilage
Authors
Issue Date1997
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/SJI
Citation
Scandinavian Journal Of Immunology, 1997, v. 45 n. 6, p. 670-677 How to Cite?
AbstractCollagen type II (CII) induced arthritis (CIA) in mice is an experimental model for rheumatoid arthritis. Induction with non-self (e.g. human) CII induces severe arthritis whereas the mice are less susceptible to induction with self CII (i.e. mouse). To analyse whether an autoimmune response to human CII can develop and is pathogenic the authors have established transgenic mice expressing human CII in cartilage and backcrossed them into two different gene backgrounds susceptible to CIA (DBA/1 and C3H.Q). The transgenic human CII expression was restricted to cartilage and did not disturb cartilage morphology or lead to chondrodystrophy. In addition, development of stress-induced arthritis was not affected by the transgene. The cartilage specific expression of human CII reduced, but did not eliminate, the susceptibility to CIA irrespective of the species source (human, bovine, chick, rat) of CII used for immunization. A common denominator between these heterologous CII in comparison with mouse CII is the previously defined CII 256-270 epitope. An expression level dependent T-cell tolerance was seen in this epitope as well as to the entire CII. However, all human transgenic mouse lines could still mount significant autoreactive T- and B-cell responses. Approximately 10% of the transgenic mice developed arthritis after immunization with human CII. These findings show, therefore, that cartilage-located human CII induce tolerance but can nevertheless be a target for development of arthritis.
Persistent Identifierhttp://hdl.handle.net/10722/147417
ISSN
2015 Impact Factor: 2.27
2015 SCImago Journal Rankings: 0.934
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMalmström, Ven_US
dc.contributor.authorHo, KKYen_US
dc.contributor.authorLun, Jen_US
dc.contributor.authorTam, PPLen_US
dc.contributor.authorCheah, KSEen_US
dc.contributor.authorHolmdahl, Ren_US
dc.date.accessioned2012-05-29T06:03:34Z-
dc.date.available2012-05-29T06:03:34Z-
dc.date.issued1997en_US
dc.identifier.citationScandinavian Journal Of Immunology, 1997, v. 45 n. 6, p. 670-677en_US
dc.identifier.issn0300-9475en_US
dc.identifier.urihttp://hdl.handle.net/10722/147417-
dc.description.abstractCollagen type II (CII) induced arthritis (CIA) in mice is an experimental model for rheumatoid arthritis. Induction with non-self (e.g. human) CII induces severe arthritis whereas the mice are less susceptible to induction with self CII (i.e. mouse). To analyse whether an autoimmune response to human CII can develop and is pathogenic the authors have established transgenic mice expressing human CII in cartilage and backcrossed them into two different gene backgrounds susceptible to CIA (DBA/1 and C3H.Q). The transgenic human CII expression was restricted to cartilage and did not disturb cartilage morphology or lead to chondrodystrophy. In addition, development of stress-induced arthritis was not affected by the transgene. The cartilage specific expression of human CII reduced, but did not eliminate, the susceptibility to CIA irrespective of the species source (human, bovine, chick, rat) of CII used for immunization. A common denominator between these heterologous CII in comparison with mouse CII is the previously defined CII 256-270 epitope. An expression level dependent T-cell tolerance was seen in this epitope as well as to the entire CII. However, all human transgenic mouse lines could still mount significant autoreactive T- and B-cell responses. Approximately 10% of the transgenic mice developed arthritis after immunization with human CII. These findings show, therefore, that cartilage-located human CII induce tolerance but can nevertheless be a target for development of arthritis.en_US
dc.languageengen_US
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/SJIen_US
dc.relation.ispartofScandinavian Journal of Immunologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshArthritis - Etiology - Genetics - Immunologyen_US
dc.subject.meshB-Lymphocytes - Immunology - Metabolismen_US
dc.subject.meshCartilage, Articular - Metabolismen_US
dc.subject.meshCattleen_US
dc.subject.meshCell Lineen_US
dc.subject.meshCollagen - Biosynthesis - Genetics - Immunologyen_US
dc.subject.meshCrosses, Geneticen_US
dc.subject.meshDisease Susceptibilityen_US
dc.subject.meshFemaleen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunoglobulins - Blooden_US
dc.subject.meshMaleen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred C3hen_US
dc.subject.meshMice, Inbred Dbaen_US
dc.subject.meshMice, Transgenicen_US
dc.subject.meshRatsen_US
dc.subject.meshT-Lymphocytes - Immunology - Metabolismen_US
dc.titleArthritis susceptibility in mice expressing human type II collagen in cartilageen_US
dc.typeArticleen_US
dc.identifier.emailCheah, KSE:hrmbdkc@hku.hken_US
dc.identifier.authorityCheah, KSE=rp00342en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid9201307-
dc.identifier.scopuseid_2-s2.0-0030920304en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0030920304&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume45en_US
dc.identifier.issue6en_US
dc.identifier.spage670en_US
dc.identifier.epage677en_US
dc.identifier.isiWOS:A1997XF25100012-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridMalmström, V=6603842874en_US
dc.identifier.scopusauthoridHo, KKY=36819420500en_US
dc.identifier.scopusauthoridLun, J=17635420800en_US
dc.identifier.scopusauthoridTam, PPL=7202539412en_US
dc.identifier.scopusauthoridCheah, KSE=35387746200en_US
dc.identifier.scopusauthoridHolmdahl, R=7103259084en_US

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