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This version published online on November 22, 2005
Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2005-1689
A more recent version of this article appeared on February 1, 2006
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*Compound via MeSH
*Substance via MeSH

Submitted on July 28, 2005
Accepted on November 16, 2005

Interferon-{gamma}-inducible {alpha}-chemokine CXCL10 involvement in Graves' ophthalmopathy: modulation by peroxisome proliferator-activated receptor-{gamma} agonists

Alessandro Antonelli*, Mario Rotondi, Silvia Martina Ferrari, Poupak Fallahi, Paola Romagnani, Stefano Sellari Franceschini, Mario Serio, and Ele Ferrannini

Department of Medicine, University of Pisa School of Medicine, Pisa; Department of Clinical and Experimental Medicine and Surgery "F. Magrassi-A. Lanzara," Second University of Naples, Naples; Department of Clinical Pathophysiology, Endocrinology Unit, University of Florence, Florence, and Otorhinolaryngology Unit, University of Pisa School of Medicine, Pisa, Italy

* To whom correspondence should be addressed. E-mail: a.antonelli{at}med.unipi.it.

Context CXC {alpha}-chemokine CXCL10/IP-10, play an important role in the initial phases of autoimmune thyroid disorders. Human thyrocytes in primary culture produce large amounts of CXCL10 when stimulated by IFN{gamma} and TNF{alpha}.

Objective Serum CXCL10 levels (sCXCL10) were measured in patients with active or inactive Graves' ophthalmopathy (GO). The effects of IFN{gamma} and TNF{alpha} stimulation and of peroxisome proliferator-activated receptor-{gamma} (PPAR{gamma}) activation, on CXCL10 secretion in primary cultures of thyrocytes, orbital fibroblasts, and preadipocytes were tested.

Patients 60 consecutive patients with Graves' disease (GD), 60 age- and sex-matched patients with GO, 60 controls.

Results sCXCL10 was higher (P < 0.0001) in GD (120 ± 83 pg/ml, n = 60) and GO (122 ± 71, n = 60) than in age- and sex-matched euthyroid controls (72 ± 32, n = 60). Among GO patients, sCXCL10 were significantly higher in those (n = 14) with active disease (171 ± 197) than with inactive disease (114 ± 45 pg/ml, P < 0.003). In primary cultures of thyrocytes, retrobulbar fibroblasts and retrobulbar preadipocytes from GO patients, CXCL10 production was absent under basal conditions; dose-dependent secretion of CXCL10 was not induced by TNF{alpha} alone, while stimulation with IFN{gamma} or TNF{alpha}+IFN{gamma} induced CXCL10 release. Treatment of all cell types with the PPAR{gamma} agonist, rosiglitazone, dose-dependently (0.1 µM-10 µM) suppressed IFN{gamma}+TNF{alpha}-induced CXCL10 release.

Conclusions We conclude that in Graves' ophthalmopathy thyrocytes and retrobulbar cell types participate in the self-perpetuation of inflammation by releasing chemokines under the influence of cytokines. PPAR{gamma} activation plays an inhibitory role in this process.
Key words: Chemokines • autoimmunity • autoantibodies




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