Skip Navigation


International Immunology Advance Access originally published online on May 28, 2009
International Immunology 2009 21(7):859-870; doi:10.1093/intimm/dxp052
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
21/7/859    most recent
dxp052v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Bharhani, M. S.
Right arrow Articles by Inman, R. D.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bharhani, M. S.
Right arrow Articles by Inman, R. D.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?


© The Japanese Society for Immunology. 2009. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Activation of invariant NKT cells confers protection against Chlamydia trachomatis-induced arthritis

Mantej Singh Bharhani, Basil Chiu, Kyoung-Sun Na and Robert D. Inman

Departments of Medicine and Immunology, Toronto Western Research Institute, University of Toronto, Toronto, Ontario, Canada

Correspondence to: R. D. Inman; E-mail: robert.inman{at}uhn.on.ca

The role of invariant NKT (iNKT) cells in reactive arthritis is unknown. We explored the functional role of NKT cells in reactive arthritis using an established murine model of Chlamydia trachomatis-induced arthritis (CtIA). CtIA in wild-type and CD1d knockout (KO) mice was induced by intra-articular injection of C. trachomatis. The effect of {alpha}-galactosylceramide ({alpha}-GalCer) activation of iNKT cells was investigated by intra-peritoneal administration of {alpha}-GalCer. Histopathological and phenotypic changes, chlamydial clearance and cytokine and chemokine production in synovial tissue of the knee joint were investigated after onset of the arthritis. The severity of CtIA was significantly increased in CD1d KO mice, which was associated with decrease in bactericidal cytokine IFN-{gamma}, regulatory cytokines IL-4 and IL-10 and increase in pro-inflammatory chemokines macrophage inflammatory protein-2 (MIP-2) and IFN-{gamma}-inducible protein-10 (IP-10). Local clearance of the pathogen from the joint was also decreased. Prior treatment of mice with {alpha}-GalCer, a potent activator of iNKT cells, significantly reduced the severity of CtIA in mice. The amelioration of CtIA was associated with decrease in chlamydial load and induction of cytokines IFN-{gamma}, IL-4 and IL-10 and significant suppression of MIP-2 and IP-10. Treatment of established CtIA with {alpha}-GalCer also demonstrated modulation of CtIA and decrease in chlamydial load. These results suggest that iNKT cells are protective against CtIA and {alpha}-GalCer-activated iNKT cells have an immunoregulatory role not only in preventing the induction of reactive arthritis but also in modulating established disease.

Keywords: {alpha}-GalCer, C. trachomatis, cytokines, iNKT cells, reactive arthritis

Transmitting editor: P. Ohashi

Received 20 December 2008, accepted 8 May 2009.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.