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Rheumatology Advance Access originally published online on July 10, 2008
Rheumatology 2008 47(9):1269-1277; doi:10.1093/rheumatology/ken257
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© The Author 2008. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

REVIEWS

Signalling, inflammation and arthritis

Crossed signals: the role of interleukin-15 and -18 in autoimmunity

H. P. Carroll1, V. Paunovic1 and M. Gadina1

1Centre for Cancer Research and Cell Biology, Queen's University Belfast, Belfast, UK.

Correspondence to: H. P. Carroll, Centre for Cancer Research and Cell Biology, Queen's University Belfast, Belfast BT9 7BL, Northern Ireland, UK. E-mail: h.carroll{at}qub.ac.uk


  Abstract

Several cytokines are involved in the complex processes ultimately leading to autoimmune diseases. In a preceding review, we have already discussed the role of the IL-12 and -17 families of cytokines. This review is focused on IL-15 and -18. Both these molecules have pro-inflammatory activity and act on many cell types and because of their broad spectrum of activity they play an important role in autoimmunity and disease pathogenesis. Their biological activity is ultimately regulated by the signalling cascades set into motion within their target cells. In this second review, we will, once again, describe the signal transduction pathways activated by these two cytokines and focus on how this relates to the pathogenesis of autoimmune diseases. We will also describe some of the therapeutic approaches that are being investigated to curtail the pro-inflammatory activities of these two molecules.

KEY WORDS: Inflammation, Cytokines, Autoimmunity, Rheumatoid arthritis, Signal transduction, Janus Kinase–Signal Transducers and Activators of Transcription pathway, Nuclear factor-{kappa}B

Submitted 1 February 2008; revised version accepted 13 June 2008.
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