Interleukin-6 stimulates thyrotropin receptor expression in human orbital preadipocyte fibroblasts from patients with Graves' ophthalmopathy

S. C. Jyonouchi, R. W. Valyasevi, D. A. Harteneck, C. M. Dutton, R. S. Bahn

Research output: Contribution to journalArticle

59 Scopus citations

Abstract

The thyrotropin receptor (TSHR) is the thyroid autoantigen against which stimulating autoantibodies are directed in Graves' hyperthyroidism. Recent evidence suggests that TSHR may also serve as an orbital autoantigen in Graves' ophthalmopathy (GO) and that expression of this protein is increased in the fatty connective tissues of the orbit in this condition. It has been shown that orbital fibroblasts from patients with GO increase thyrotropin (TSH)-dependent cyclic adenosine monophosphate (cAMP) production and TSHR gene expression when cultured under conditions known to stimulate adipocyte differentiation. In the current study, we wanted to determine whether treatment of these cells with particular cytokines (each 1 ng/mL) during differentiation might further augment TSHR expression. We found that exposure to interleukin (IL)-6 increased TSHR expression above control levels in cells from patients with GO. In contrast, this cytokine did not affect TSHR expression in normal orbital cells. Neither IL-4 nor IL-1α had a significant stimulatory effect in either normal or Graves' cultures. These findings suggest that IL-6 may play a role in the pathogenesis of GO by increasing expression of the putative autoantigen within the adipose/connective tissues of the orbit.

Original languageEnglish (US)
Pages (from-to)929-934
Number of pages6
JournalThyroid
Volume11
Issue number10
DOIs
StatePublished - Jan 1 2001

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

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