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Rheumatology Advance Access originally published online on February 16, 2007
Rheumatology 2007 46(4):565-571; doi:10.1093/rheumatology/kel437
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© The Author 2007. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org


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NKT cells: manipulable managers of joint inflammation

K. Coppieters, P. Dewint, K. Van Beneden, P. Jacques, S. Seeuws, G. Verbruggen, D. Deforce1 and D. Elewaut

Laboratory for Molecular Immunology & Inflammation, Department of Rheumatology, Ghent University Hospital and 1Laboratory for Pharmaceutical Biotechnology, Ghent University, Ghent, Belgium

Correspondence to: Dirk Elewaut, Ghent University Hospital Laboratory for Molecular Immunology and Inflammation, Department of Rheumatology, 185 De Pintelaan, B-9000 Ghent, Belgium. E-mail: Dirk.Elewaut{at}UGent.be


   Abstract

The importance of T cell participation in the aetiology and pathogenesis of rheumatoid arthritis (RA) is now widely appreciated. The disease is mediated by activated pro-inflammatory, self-reactive T helper cells, instigating the chronic autoimmune response characteristic of rheumatoid inflammation. Natural killer T (NKT) cells are a distinctive population of T cells thought to protect self-tissues from damaging inflammatory immune responses, and are often recognized as a regulatory T cell subtype, regulating the magnitude or class of the immune response. Recently, a number of studies have provided insight concerning the role of NKT cells in different models of autoimmune joint inflammation, suggesting the involvement of this specialized T cell subset in controlling initiation and perpetuation of arthritic disease. The aim of this review is to provide rheumatologists with an introduction of the principal features of NKT cells, to give an overview of the data obtained in animal models of arthritis and to discuss the hypothesized mechanisms. Finally, we will speculate on future prospects with regard to NKT cell-targeted treatment of arthritic disease by use of glycolipids.

KEY WORDS: Rheumatoid arthritis, NKT cells, Cytokines, Inflammation, Mouse, Autoimmunity

Submitted 4 November 2006; revised version accepted 8 December 2006.
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