Browse

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

Cited 101 time in Web of Science Cited 109 time in Scopus
Authors
Kim, Hye Young; Kim, Hyun Jung; Min, Hye Sook; Kim, Sanghee; Park, Weon Seo; Park, Seong Hoe; Chung, Doo Hyun
Issue Date
2005-01-03
Publisher
Rockefeller University Press
Citation
J. Exp. Med. 2005;201(1):41-47.
Keywords
AnimalsAntibodies, Monoclonal/metabolismArthritis/*etiology/immunology/metabolismDNA PrimersEnzyme-Linked Immunosorbent AssayGalactosylceramides/*pharmacologyInterferon-gamma/metabolismInterleukin-4/metabolismKiller Cells, Natural/*drug effects/metabolismLymphocyte Activation/drug effectsMiceMice, Mutant StrainsReverse Transcriptase Polymerase Chain ReactionT-Lymphocyte Subsets/*drug effects/metabolismTransforming 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

http://hdl.handle.net/10371/10005
DOI
https://doi.org/10.1084/jem.20041400
Files in This Item:
Appears in Collections:
College of Medicine/School of Medicine (의과대학/대학원)Pathology (병리학전공)Journal Papers (저널논문_병리학전공)
  • mendeley

Items in S-Space are protected by copyright, with all rights reserved, unless otherwise indicated.

Browse