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Article: Chondrocyte antigen expression, immune response and susceptibility to arthritis

TitleChondrocyte antigen expression, immune response and susceptibility to arthritis
Authors
Keywordsβ-Galactosidase
Ankylosing spondylitis
Autoimmunity
BALB/c
Collagen
Cytotoxic T lymphocyte
Influenza A virus
Mice
Nucleoprotein
Rodent
Tolerance
Issue Date2001
PublisherOxford University Press. The Journal's web site is located at http://intimm.oxfordjournals.org/
Citation
International Immunology, 2001, v. 13 n. 4, p. 421-429 How to Cite?
AbstractThe association of HLA-B27 with certain forms of arthritis implies a role for MHC class I-restricted T cells in the arthritic process. Our aim was to study CD8+ T cell responses towards specific antigens localized in joint tissue. Known determinants were introduced into chondrocytes of transgenic (TG) mice, under the control of the cis-regulatory sequences of the human type II collagen gene (COL2A1). Two Escherichia coli β-galactosidase (β-gal)-expressing lines were derived (CIIL73 and CIIL64) as well as two lines (CIINP) expressing influenza A virus nucleoprotein (NP). Expression of the antigens could be demonstrated in cartilaginous tissues. The TG lines showed variable degrees of responsiveness towards the transgene-introduced antigens; whilst 75% of CIIL73 mice had an imparied cytotoxic T lymphocyte (CTL) response towards β-gal, the response in CIIL64 mice was essentially normal. However, both lines displayed normal proliferative and antibody responses to β-gal. A reduced CTL responses was seen to NP in the CIINP lines in ∼65% of the animals. In spite of the persistence of T cells responses to the transgene antigens in these lines, induction of CTL responses alone has so far failed to induce clinical signs of arthritis. Interestingly, some animals expressing β-gal were susceptible to arthritis following challenge with type II collagen alone, whilst their non-TG littermates and TG mice from other lines remained unaffected. As β-gal is expressed by E. coli, a component of the normal gut flora, this suggests a possible role for gut-derived immune responses. We believe these lines could form the basis of a model for studying links between intestinal inflammation and arthritis.
Persistent Identifierhttp://hdl.handle.net/10722/132502
ISSN
2015 Impact Factor: 3.031
2015 SCImago Journal Rankings: 1.613
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChan, VSFen_HK
dc.contributor.authorCohen, ESen_HK
dc.contributor.authorWeissensteiner, Ten_HK
dc.contributor.authorCheah, KSEen_HK
dc.contributor.authorBodmer, HCen_HK
dc.date.accessioned2011-03-28T09:25:28Z-
dc.date.available2011-03-28T09:25:28Z-
dc.date.issued2001en_HK
dc.identifier.citationInternational Immunology, 2001, v. 13 n. 4, p. 421-429en_HK
dc.identifier.issn0953-8178en_HK
dc.identifier.urihttp://hdl.handle.net/10722/132502-
dc.description.abstractThe association of HLA-B27 with certain forms of arthritis implies a role for MHC class I-restricted T cells in the arthritic process. Our aim was to study CD8+ T cell responses towards specific antigens localized in joint tissue. Known determinants were introduced into chondrocytes of transgenic (TG) mice, under the control of the cis-regulatory sequences of the human type II collagen gene (COL2A1). Two Escherichia coli β-galactosidase (β-gal)-expressing lines were derived (CIIL73 and CIIL64) as well as two lines (CIINP) expressing influenza A virus nucleoprotein (NP). Expression of the antigens could be demonstrated in cartilaginous tissues. The TG lines showed variable degrees of responsiveness towards the transgene-introduced antigens; whilst 75% of CIIL73 mice had an imparied cytotoxic T lymphocyte (CTL) response towards β-gal, the response in CIIL64 mice was essentially normal. However, both lines displayed normal proliferative and antibody responses to β-gal. A reduced CTL responses was seen to NP in the CIINP lines in ∼65% of the animals. In spite of the persistence of T cells responses to the transgene antigens in these lines, induction of CTL responses alone has so far failed to induce clinical signs of arthritis. Interestingly, some animals expressing β-gal were susceptible to arthritis following challenge with type II collagen alone, whilst their non-TG littermates and TG mice from other lines remained unaffected. As β-gal is expressed by E. coli, a component of the normal gut flora, this suggests a possible role for gut-derived immune responses. We believe these lines could form the basis of a model for studying links between intestinal inflammation and arthritis.en_HK
dc.languageengen_US
dc.publisherOxford University Press. The Journal's web site is located at http://intimm.oxfordjournals.org/en_HK
dc.relation.ispartofInternational Immunologyen_HK
dc.rightsInternational Immunology. Copyright © Oxford University Press.-
dc.subjectβ-Galactosidaseen_HK
dc.subjectAnkylosing spondylitisen_HK
dc.subjectAutoimmunityen_HK
dc.subjectBALB/cen_HK
dc.subjectCollagenen_HK
dc.subjectCytotoxic T lymphocyteen_HK
dc.subjectInfluenza A virusen_HK
dc.subjectMiceen_HK
dc.subjectNucleoproteinen_HK
dc.subjectRodenten_HK
dc.subjectToleranceen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAnimals, Newbornen_HK
dc.subject.meshAntibodiesen_HK
dc.subject.meshArthritis - etiology - immunologyen_HK
dc.subject.meshCartilage, Articular - immunologyen_HK
dc.subject.meshChondrocytes - immunologyen_HK
dc.subject.meshCollagen - geneticsen_HK
dc.subject.meshDisease Susceptibilityen_HK
dc.subject.meshEscherichia coli - geneticsen_HK
dc.subject.meshGenetic Vectorsen_HK
dc.subject.meshHumansen_HK
dc.subject.meshImmunizationen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Inbred BALB Cen_HK
dc.subject.meshMice, Inbred C57BLen_HK
dc.subject.meshMice, Transgenicen_HK
dc.subject.meshNucleoproteins - biosynthesis - immunologyen_HK
dc.subject.meshRNA-Binding Proteinsen_HK
dc.subject.meshT-Lymphocytes, Cytotoxicen_HK
dc.subject.meshViral Core Proteins - biosynthesis - immunologyen_HK
dc.subject.meshbeta-Galactosidase - biosynthesis - immunologyen_HK
dc.titleChondrocyte antigen expression, immune response and susceptibility to arthritisen_HK
dc.typeArticleen_HK
dc.identifier.emailChan, VSF:sfvchan@hku.hken_HK
dc.identifier.emailCheah, KSE:hrmbdkc@hku.hken_HK
dc.identifier.authorityChan, VSF=rp01459en_HK
dc.identifier.authorityCheah, KSE=rp00342en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid11282981-
dc.identifier.scopuseid_2-s2.0-0035073417en_HK
dc.identifier.hkuros58495-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035073417&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume13en_HK
dc.identifier.issue4en_HK
dc.identifier.spage421en_HK
dc.identifier.epage429en_HK
dc.identifier.isiWOS:000168062500003-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridChan, VSF=35200370000en_HK
dc.identifier.scopusauthoridCohen, ES=18834378400en_HK
dc.identifier.scopusauthoridWeissensteiner, T=6601933901en_HK
dc.identifier.scopusauthoridCheah, KSE=35387746200en_HK
dc.identifier.scopusauthoridBodmer, HC=6701765081en_HK

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