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pubmed-article:21371758pubmed:abstractTextAutoimmune thyroid disease (AITD) has been reported in patients with multiple sclerosis (MS) receiving interferon-beta (IFN-?), but not in those receiving Glatiramer acetate (GA). CXCL10 is a chemokine playing a pathogenetic role in AITD and MS. Our aim was to evaluate the effects on CXCL10 secretion of IFN-? and GA, alone and in combination with TNF-?, in primary cultures of thyrocytes (PCT). Significant and dose-dependent secretions of CXCL10 were induced by IFN-? but not GA. TNF-? synergistically increased IFN-? induced CXCL10 secretion. These results may provide an explanation for the occurrence of AITD during IFN-?, but not during GA, treatment for MS.lld:pubmed
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pubmed-article:21371758pubmed:copyrightInfoCopyright © 2011 Elsevier B.V. All rights reserved.lld:pubmed
pubmed-article:21371758pubmed:issnTypeElectroniclld:pubmed
pubmed-article:21371758pubmed:volume234lld:pubmed
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pubmed-article:21371758pubmed:articleTitleInterferon-? but not Glatiramer acetate stimulates CXCL10 secretion in primary cultures of thyrocytes: a clue for understanding the different risks of thyroid dysfunctions in patients with multiple sclerosis treated with either of the two drugs.lld:pubmed
pubmed-article:21371758pubmed:affiliationUnit of Internal Medicine and Endocrinology, Fondazione Salvatore Maugeri I.R.C.C.S., ISPESL Laboratory for Endocrine Disruptors and Chair of Endocrinology, University of Pavia, Italy.lld:pubmed
pubmed-article:21371758pubmed:publicationTypeJournal Articlelld:pubmed