Open AccessHypothyroidism in transgenic mice expressing IFN-γ in the thyroid
Author(s) -
Patrizio Caturegli,
Mehrdad Hejazi,
Koichi Suzuki,
Orsolya Dohán,
Nancy Carrasco,
Leonard D. Kohn,
Noel R. Rose
Publication year - 2000
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.020522597
Subject(s) - thyroid , thyroiditis , sodium iodide symporter , endocrinology , medicine , autoimmune thyroiditis , genetically modified mouse , transgene , symporter , biology , gene , transporter , biochemistry
IFN-γ has been implicated with contradictory results in the pathogenetic process of autoimmune (Hashimoto's) thyroiditis, the most common cause of hypothyroidism in adults. To test whether the local production of IFN-γ can lead to thyroid dysfunction, we have generated transgenic mice that express constitutively IFN-γ in the thyroid follicular cells. This expression resulted in severe hypothyroidism, with growth retardation and disruption of the thyroid architecture. The hypothyroidism derived from a profound inhibition of the expression of the sodium iodide symporter gene. Taken together, these results indicate a direct role of IFN-γ in the thyroid dysfunction that occurs in autoimmune thyroiditis.