Abstract
Abstract It has been known for over three decades that thyroid stimulating hormone (TSH) is made by cells of the immune system, yet little is known about the biological significance of that. Studies in my laboratory identified a novel splice variant of the TSH β-subunit (TSHβv) that is produced by bone marrow (BM) hematopoietic cells and peripheral leukocytes in humans and mice. As shown here, recombinant mouse TSHβ (rTSHβ) binds in a dose-dependent manner to the TSH receptor (TSHR) on the mouse AM macrophage cell line, and circulating T4 levels are suppressed 38% in mice 24 hrs after injection of rTSHβv. Moreover, TSHβ-producing leukocytes traffic to the thyroid during systemic L. monocytogenes infection. TSHβv is suppressed in mouse macrophages following transfection with short-hairpin RNA TSHβv (shRNA-TSHβv) expression plasmids, and is suppressed in BM cells transduced with shRNA-TSHβv lentivirus pseudoparticles. These findings collectively suggest that binding of immune system TSHβv to the TSHR on thyroid follicular cells may serve to modulate thyroid hormone output, thus providing a novel mechanism for regulating host metabolism during times of immune stress. Experiments are underway in mice to understand the in vivo involvement of immune system TSHβv in healthy conditions, and during chronic inflammation such as in autoimmune thyroiditis.
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