Interferon-α Triggers Autoimmune Thyroid Diseases via Lysosomal-Dependent Degradation of Thyroglobulin
Author(s) -
Larissa C. Faustino,
Angela Lombardi,
Julio MadrigalMatute,
Randall P. Owen,
Steven K. Libutti,
Yaron Tomer
Publication year - 2018
Publication title -
the journal of clinical endocrinology and metabolism
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 2.206
H-Index - 353
eISSN - 1945-7197
pISSN - 0021-972X
DOI - 10.1210/jc.2018-00541
Subject(s) - thyroglobulin , endocrinology , autophagy , medicine , xbp1 , thyroid , thyroiditis , protein degradation , downregulation and upregulation , endoplasmic reticulum , interferon , biology , chemistry , immunology , microbiology and biotechnology , gene , biochemistry , rna , apoptosis , rna splicing
Autoimmune thyroid diseases (AITDs) arise from complex interactions among genetic, epigenetic, and environmental factors. Thyroglobulin (TG) is a major susceptibility gene for both Graves disease and Hashimoto thyroiditis. Interferon-α (IFNα), a cytokine secreted during viral infections, has emerged as a key trigger of AITD. We have shown that IFNα upregulates TG transcription; however, how the upregulation of TG transcription by IFNα triggers AITD is still unknown.
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