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Rheumatology Advance Access originally published online on March 20, 2008
Rheumatology 2008 47(6):753-759; doi:10.1093/rheumatology/ken053
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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


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Interleukin-7 in rheumatoid arthritis

S. M. Churchman and F. Ponchel

The University of Leeds, Leeds Institute of Molecular Medicine, Section of Musculoskeletal Disease, St James's University Hospital, Leeds, UK.

Correspondence to: F. Ponchel, The University of Leeds, Leeds Institute of Molecular Medicine, Section of Musculoskeletal Disease, St James's University Hospital, Leeds, LS9 7TF, UK. E-mail: f.ponchel{at}leeds.ac.uk; mmefp{at}leeds.ac.uk


   Abstract

Recent data from several groups demonstrate high levels of IL-7 in the joints of RA patients, but much lower levels in OA. In contrast, circulating levels of IL-7 in RA remain a point of debate. IL-7 has many roles in T cell, dendritic cell and bone biology in humans. Reduced levels of circulating IL-7 probably underlie a number of the dysfunctions associated with circulating T cells in RA and may provide a mechanism for some of the unexplained systemic manifestations of the disease. However, IL-7 in the joint may have a more sinister role, contributing to a vicious cycle perpetuating inflammation. Typically, IL-1β and TNF-{alpha} increase the stromal production of IL-7 and in turn, IL-7 up-regulates the production of TNF-{alpha} by macrophages. Most importantly, IL-7 induces the production of osteoclastogenic cytokines by T cells, leading to the maturation of osteoclasts and therefore bone destruction. By linking the stroma with innate and adaptive immunity in RA, IL-7 may be directing the cellular network, leading to chronic inflammation and joint destruction. Blocking IL-7 may well therefore be of therapeutic value.

KEY WORDS: IL-7, RA, Inflammation, T cells

Submitted 19 July 2007; revised version accepted 23 January 2008.
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