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Bone marrow cells produce a novel TSHβ splice variant that is upregulated in the thyroid following systemic virus infection
Journal article   Open access   Peer reviewed

Bone marrow cells produce a novel TSHβ splice variant that is upregulated in the thyroid following systemic virus infection

Bryce H. Vincent, Dina Montufar-Solis, Ba-Bie Teng, Brad A. Amendt, Jeremy Schaefer and John R. Klein
Genes and immunity, Vol.10(1), pp.18-26
08/28/2008
DOI: 10.1038/gene.2008.69
PMCID: PMC2629504
PMID: 18754015
url
https://doi.org/10.1038/gene.2008.69View
Published (Version of record) Open Access

Abstract

Although cells of the immune system can produce thyroid stimulating hormone (TSH), the significance of that remains unclear. Using 5′ rapid amplification of cDNA ends, we show that mouse bone marrow cells produce a novel in-frame TSHβ splice variant generated from a portion of intron 4 with all of the coding region of exon 5 but none of exon 4. The TSHβ splice variant gene was expressed at low levels in the pituitary but at high levels in the bone marrow and the thyroid, and the protein was secreted from transfected CHO cells. Immunoprecipitation identified an 8 kDa product in lysates of CHO cells transfected with the novel TSHβ construct, and a 17 kDa product in lysates of CHO cells transfected with the native TSHβ construct. The splice variant TSHβ protein elicited a cAMP response from FRTL-5 thyroid follicular cells and a mouse alveolar macrophage cell line. Expression of the TSHβ splice variant but not the native form of TSHβ was significantly upregulated in the thyroid during systemic virus infection. These studies characterize the first functional splice variant of TSHβ, which may contribute to the metabolic regulation during immunological stress, and may offer an new perspective for understanding autoimmune thyroiditis.
5′ RACE analysis autoimmunity isoform metabolism thyrotropin

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