Interferon-β 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

Mario Rotondi, Francesca Stufano, Maria Stefania Lagonigro, Luigi La Manna, Francesca Zerbini, Stefania Ghilotti, Maria Teresa Pagliari, Francesca Coperchini, Flavia Magri, Roberto Bergamaschi, Antonio Oliviero, Luca Chiovato

Research output: Contribution to journalArticlepeer-review

Abstract

Autoimmune thyroid disease (AITD) has been reported in patients with multiple sclerosis (MS) receiving interferon-beta (IFN-β), 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-β and GA, alone and in combination with TNF-α, in primary cultures of thyrocytes (PCT). Significant and dose-dependent secretions of CXCL10 were induced by IFN-β but not GA. TNF-α synergistically increased IFN-β induced CXCL10 secretion. These results may provide an explanation for the occurrence of AITD during IFN-β, but not during GA, treatment for MS.

Original languageEnglish
Pages (from-to)161-164
Number of pages4
JournalJournal of Neuroimmunology
Volume234
Issue number1-2
DOIs
Publication statusPublished - May 2011

Keywords

  • Autoimmunity
  • Chemokines
  • CXCL10
  • Glatiramer acetate
  • Interferons
  • Thyrocytes

ASJC Scopus subject areas

  • Immunology
  • Clinical Neurology
  • Immunology and Allergy
  • Neurology

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