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NKT cells promote antibody-induced joint inflammation by suppressing transforming growth factor beta1 production
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Kim, H. Y. | - |
dc.contributor.author | Kim, H. J. | - |
dc.contributor.author | Min, H. S. | - |
dc.contributor.author | Kim, S. | - |
dc.contributor.author | Park, W. S. | - |
dc.contributor.author | Park, S. H. | - |
dc.contributor.author | Chung, D. H. | - |
dc.date.accessioned | 2009-12-24T11:24:26Z | - |
dc.date.available | 2009-12-24T11:24:26Z | - |
dc.date.issued | 2005-01-05 | - |
dc.identifier.citation | J Exp Med. 2005 Jan 3;201(1):41-7. | en |
dc.identifier.issn | 0022-1007 (Print) | - |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15630137 | - |
dc.identifier.uri | https://hdl.handle.net/10371/22623 | - |
dc.description.abstract | Although 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.iso | en | en |
dc.publisher | Rockefeller University Press | en |
dc.subject | Animals | en |
dc.subject | Antibodies, Monoclonal/metabolism | en |
dc.subject | Arthritis/*etiology/immunology/metabolism | en |
dc.subject | DNA Primers | en |
dc.subject | Enzyme-Linked Immunosorbent Assay | en |
dc.subject | Galactosylceramides/*pharmacology | en |
dc.subject | Interferon-gamma/metabolism | en |
dc.subject | Interleukin-4/metabolism | en |
dc.subject | Killer Cells, Natural/*drug effects/metabolism | en |
dc.subject | Lymphocyte Activation/drug effects | en |
dc.subject | Mice | en |
dc.subject | Mice, Mutant Strains | en |
dc.subject | Reverse Transcriptase Polymerase Chain Reaction | en |
dc.subject | T-Lymphocyte Subsets/*drug effects/metabolism | en |
dc.subject | Transforming Growth Factor beta/*metabolism | en |
dc.title | NKT cells promote antibody-induced joint inflammation by suppressing transforming growth factor beta1 production | en |
dc.type | Article | en |
dc.contributor.AlternativeAuthor | 김혜영 | - |
dc.contributor.AlternativeAuthor | 김현정 | - |
dc.contributor.AlternativeAuthor | 민혜숙 | - |
dc.contributor.AlternativeAuthor | 김상희 | - |
dc.contributor.AlternativeAuthor | 박원서 | - |
dc.contributor.AlternativeAuthor | 박성회 | - |
dc.contributor.AlternativeAuthor | 정두현 | - |
dc.identifier.doi | 10.1084/jem.20041400 | - |
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