Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2011-5-11
pubmed:abstractText
Autoimmune 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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1872-8421
pubmed:author
pubmed:copyrightInfo
Copyright © 2011 Elsevier B.V. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
234
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
161-4
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Interferon-? 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.
pubmed:affiliation
Unit 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.
pubmed:publicationType
Journal Article