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NKT cells promote antibody-induced joint inflammation by suppressing transforming growth factor beta1 production
Cited 107 time in
Web of Science
Cited 117 time in Scopus
- Authors
- Issue Date
- 2005-01-05
- Publisher
- Rockefeller University Press
- Citation
- J Exp Med. 2005 Jan 3;201(1):41-7.
- Keywords
- Animals ; Antibodies, Monoclonal/metabolism ; Arthritis/*etiology/immunology/metabolism ; DNA Primers ; Enzyme-Linked Immunosorbent Assay ; Galactosylceramides/*pharmacology ; Interferon-gamma/metabolism ; Interleukin-4/metabolism ; Killer Cells, Natural/*drug effects/metabolism ; Lymphocyte Activation/drug effects ; Mice ; Mice, Mutant Strains ; Reverse Transcriptase Polymerase Chain Reaction ; T-Lymphocyte Subsets/*drug effects/metabolism ; Transforming Growth Factor beta/*metabolism
- 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.
- ISSN
- 0022-1007 (Print)
- Language
- English
- URI
- http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15630137
https://hdl.handle.net/10371/22623
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