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FcgammaRIII engagement provides activating signals to NKT cells in antibody-induced joint inflammation

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dc.contributor.authorKim, H. Y.-
dc.contributor.authorKim, S.-
dc.contributor.authorChung, D. H.-
dc.date.accessioned2009-12-24T10:52:36Z-
dc.date.available2009-12-24T10:52:36Z-
dc.date.issued2006-08-19-
dc.identifier.citationJ Clin Invest. 2006 Sep;116(9):2484-92. Epub 2006 Aug 17.en
dc.identifier.issn0021-9738 (Print)-
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16917543-
dc.identifier.urihttps://hdl.handle.net/10371/22586-
dc.description.abstractNKT cells promote antibody-induced arthritis, but the mechanism by which NKT cells are activated in this model remains unclear. It has been proposed that Fcgamma receptor (FcgammaR) contributes to NKT cell activation in antibody-induced arthritis. To address this issue, we explored the functions of FcgammaR on NKT cells in antibody-induced arthritis. RT-PCR and flow cytometric analysis demonstrated that NKT cells constitutively express surface FcgammaRIII but not FcgammaRI, -II, or -IV. FcgammaRIII engagement by aggregated IgG on NKT cells enhanced CD25 and CD69 expression, whereas FcgammaR(-/-) mouse NKT cells did not enhance activation. FcgammaRIII engagement on NKT cells enhanced the production of IL-4, IL-10, IL-13, and IFN-gamma, whereas FcgammaR-deficient NKT cells did not alter the production of these cytokines after aggregated IgG treatment. However, FcgammaR-deficient NKT cells were functionally intact in terms of TCR-induced activation. Moreover, adoptive transfer of FcgammaR-deficient NKT cells could not restore inflammation or TGF-beta production in the joint tissues of CD1d(-/-) mice, whereas adoptive transfer of wild-type NKT cells induced arthritis and reduced TGF-beta production in joint tissues. We conclude that FcgammaRIII engagement by IgG in joint tissues provides activating signals to NKT cells in antibody-induced arthritis.en
dc.language.isoen-
dc.publisherAmerican Society for Clinical Investigationen
dc.subjectAdoptive Transferen
dc.subjectAnimalsen
dc.subjectArthritis, Experimental/*immunologyen
dc.subjectCell Lineen
dc.subjectDNA Primersen
dc.subjectImmunoglobulin G/immunologyen
dc.subjectInflammation/immunologyen
dc.subjectInterferon-gamma/biosynthesisen
dc.subjectInterleukins/biosynthesisen
dc.subjectJoint Diseases/immunologyen
dc.subjectKiller Cells, Natural/*immunologyen
dc.subjectMiceen
dc.subjectMice, Inbred NODen
dc.subjectMice, Transgenicen
dc.subjectReceptors, IgG/deficiency/genetics/*physiologyen
dc.subjectReverse Transcriptase Polymerase Chain Reactionen
dc.subjectT-Lymphocyte Subsets/*immunologyen
dc.subjectT-Lymphocytes, Regulatory/immunologyen
dc.titleFcgammaRIII engagement provides activating signals to NKT cells in antibody-induced joint inflammationen
dc.typeArticleen
dc.contributor.AlternativeAuthor김혜영-
dc.contributor.AlternativeAuthor김상희-
dc.contributor.AlternativeAuthor정두현-
dc.identifier.doi10.1172/JCI27219-
Appears in Collections:
College of Medicine/School of Medicine (의과대학/대학원)Immunology (면역학전공)Journal Papers (저널논문_면역학전공)
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