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NKT cells promote antibody-induced joint inflammation by suppressing transforming growth factor beta1 production

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dc.contributor.authorKim, Hye Young-
dc.contributor.authorKim, Hyun Jung-
dc.contributor.authorMin, Hye Sook-
dc.contributor.authorKim, Sanghee-
dc.contributor.authorPark, Weon Seo-
dc.contributor.authorPark, Seong Hoe-
dc.contributor.authorChung, Doo Hyun-
dc.date.accessioned2009-10-01T03:02:13Z-
dc.date.available2009-10-01T03:02:13Z-
dc.date.issued2005-01-03-
dc.identifier.citationJ. Exp. Med. 2005;201(1):41-47.en
dc.identifier.issn0022-1007 (Print)-
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15630137-
dc.identifier.urihttp://hdl.handle.net/10371/10005-
dc.description.abstractAlthough NKT cells has been known to exert protective roles in the development of autoimmune diseases, the functional roles of NKT cells in the downstream events of antibody-induced joint inflammation remain unknown. Thus, we explored the functional roles of NKT cells in antibody-induced arthritis using the K/BxN serum transfer model. NKT cell-deficient mice were resistant to the development of arthritis, and wild-type mice administrated with alpha-galactosyl ceramide, a potent NKT cell activator, aggravated arthritis. In CD1d-/- mice, transforming growth factor (TGF)-beta1 was found to be elevated in joint tissues, and the blockade of TGF-beta1 using neutralizing monoclonal antibodies restored arthritis. The administration of recombinant TGF-beta1 into C57BL/6 mice reduced joint inflammation. Moreover, the adoptive transfer of NKT cells into CD1d-/- mice restored arthritis and reduced TGF-beta1 production. In vitro assay demonstrated that interleukin (IL)-4 and interferon (IFN)-gamma were involved in suppressing TGF-beta1 production in joint cells. The adoptive transfer of NKT cells from IL-4-/- or IFN-gamma-/- mice did not reverse arthritis and TGF-beta1 production in CD1d-/- mice. In conclusion, NKT cells producing IL-4 and IFN-gamma play a role in immune complex-induced joint inflammation by regulating TGF-beta1.en
dc.language.isoenen
dc.publisherRockefeller University Pressen
dc.subjectAnimalsen
dc.subjectAntibodies, Monoclonal/metabolismen
dc.subjectArthritis/*etiology/immunology/metabolismen
dc.subjectDNA Primersen
dc.subjectEnzyme-Linked Immunosorbent Assayen
dc.subjectGalactosylceramides/*pharmacologyen
dc.subjectInterferon-gamma/metabolismen
dc.subjectInterleukin-4/metabolismen
dc.subjectKiller Cells, Natural/*drug effects/metabolismen
dc.subjectLymphocyte Activation/drug effectsen
dc.subjectMiceen
dc.subjectMice, Mutant Strainsen
dc.subjectReverse Transcriptase Polymerase Chain Reactionen
dc.subjectT-Lymphocyte Subsets/*drug effects/metabolismen
dc.subjectTransforming Growth Factor beta/*metabolismen
dc.titleNKT cells promote antibody-induced joint inflammation by suppressing transforming growth factor beta1 productionen
dc.typeArticleen
dc.contributor.AlternativeAuthor김혜영-
dc.contributor.AlternativeAuthor김현정-
dc.contributor.AlternativeAuthor민혜숙-
dc.contributor.AlternativeAuthor김상희-
dc.contributor.AlternativeAuthor박원서-
dc.contributor.AlternativeAuthor박성회-
dc.contributor.AlternativeAuthor정두현-
dc.identifier.doi10.1084/jem.20041400-
Appears in Collections:
College of Medicine/School of Medicine (의과대학/대학원)Pathology (병리학전공)Journal Papers (저널논문_병리학전공)
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