Rheumatology Advance Access published online on February 11, 2008
Rheumatology, doi:10.1093/rheumatology/kem389
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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
Editorial |
Leptin and ANCA-associated vasculitis: a healthy link?
Cardiovascular Research Institute Maastricht (CARIM), Department of Internal Medicine, Division of Clinical and Experimental Immunology, Maastricht University, Maastricht, The Netherlands
Correspondence to:
Correspondence to: J. W. Cohen Tervaert, University of Maastricht, PO Box 616, 6200 MD Maastricht, The Netherlands. E-mail: jw.cohentervaert@immuno.unimaas.nl
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Leptin is a 16-kDa peptide hormone that is mainly produced by adipocytes. It structurally resembles the pro-inflammatory cytokines IL-6 and IL-12. Leptin has been recognized as a key factor regulating body weight by inhibiting food intake and stimulating energy expenditure. In addition, leptin exerts pleiotropic actions in modulating immune responses. It activates monocytes and macrophages and contributes to the maturation and survival of dendritic cells. Importantly, leptin has also been shown to modulate the adaptive immune system, via enhancing T-cell survival and skewing T-cell differentiation towards a Th1 response. Recently, several papers demonstrated that leptin also affects homeostasis and function of CD4+CD25+ regulatory T (Treg) cells. Therefore, leptin dysregulation may be involved in the pathogenesis of autoimmune diseases such as ANCA-associated vasculitis.
Treg cells in autoimmune diseases
Autoimmune diseases are initiated by a loss of immunological tolerance to self antigens. The generation of autoreactive T and
Leptin and Treg cells
Leptin levels in autoimmune disease
Leptin and ANCA-associated vasculitis
Conclusion