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Hormones as Immune Modulating Agents
Published in Thomas F. Kresina, Immune Modulating Agents, 2020
The stimulation of human monocytes in vitro with TRH induced TSH release which could be totally inhibited by the administration of triiodothyronine (T3) [303]. Human lymphocytes synthesized the β subunit of TSH. The messenger RNA for the TSHβ subunit was regulated by thyromimetic compounds [304].
Nonautoimmune thyroid disease
Published in Philip E. Harris, Pierre-Marc G. Bouloux, Endocrinology in Clinical Practice, 2014
Arie Berghout, Alex F. Muller, Philip E. Harris
Although antithyroid drugs may be considered for patients with features of thyrotoxicosis, they may be associated with a further rise in TSH levels, overriding their effects, with an increase in the size of a goiter. Thyroid hormone analogues such as TRIAC (3,3,5-triiodothyroacetic acid) may be used. TRIAC has has predominantly pituitary and hepatic thyromimetic effects—tissues that are relatively refractory to thyroid hormones in RTH, and it has a preferential affinity for TRβ in vitro86 The Food and Drug Administration (FDA) has issued several health warnings referring to the use of TRIAC for nonmedical reasons, such as weight loss and reduction in body fat in body builders. Patients who cannot be controlled with TRIAC alone may respond to combined therapy with an antithyroid drugs such as carbimazole/methimazole.87 An alternative therapy that may be considered is with dextrothyroxine (D-T4).
Neuroendocrine Peptide Hormones and Receptors in the Immune Response and Infectious Diseases
Published in Herman Friedman, Thomas W. Klein, Andrea L. Friedman, Psychoneuroimmunology, Stress, and Infection, 2020
Douglas A. Weigent, J. Edwin Blalock
Shortly after the discovery that human lymphocytes produce ACTH, it was observed they also could generate TSH. Stimulation of human PBL with staphylococcal enterotoxin A (SEA), a T cell mitogen, increased TSH beta subunit-specific immunofluorescence.26 In this study, it was also shown that lymphocyte TSH was de novo synthesized and had a similar subunit structure to pituitary TSH. The TSH-β-related RNA was detected in human and mouse lymphocytes.27 The production of TSH has also been studied in cell lines where a transcript the same size as pituitary TSH was detected in the T cell lymphoma line Hut-78.28 The production of TSH in this cell line was increased by thyrotropin-releasing hormone and reduced by triiodothyronine. In a more recent report, the TSH β-subunit has been amplified from a human lymphoma cell line (WIL2) and the nucleotide sequence analysis suggests it is not identical to pituitary TSH.29 Interestingly, only a 3% difference was found which had no effect on the amino acid sequence. These mostly silent changes were not observed at the exonintron boundaries. The results from this latter study confirmed the effect of thyromimetic compounds on the expression of TSH-β-RNA. Besides TSH, two other glycoprotein hormones once thought to be restricted to the pituitary have been identified in the immune system. In response to luteinizing hormone releasing hormone (LHRH), lymphocytes from humans and mice produced and secreted an immunoreactive LH.30,31 The lymphocyte-derived LH was similar to the pituitary hormone in subunit structure and antigenicity.32 Two biologically active immunoreactive follicle-stimulating hormones (FSH) have been detected with different molecular weights after treatment of rat lymphocytes with the T cell mitogen, concanavalin A.33 One form was similar to pituitary FSH while the other was larger. Both bone marrow and the spleen produce inhibin and activin and it remains to be determined whether these hormones play a role in the lymphoid levels of FSH.34
Thyromimetics as emerging therapeutic agents for nonalcoholic steatohepatitis: rationale for the development of resmetirom (MGL-3196)
Published in Expert Opinion on Investigational Drugs, 2020
Therefore, selectivity for a thyromimetic at the THR-β isoform, the predominant liver THR, has the potential of providing the metabolic benefits of thyroid hormone and at the same time avoiding unwanted systemic actions in the heart and bones that are largely mediated through the THR-α isoform [11]. Other pharmacologic strategies to target the thyroid-liver axis include the use of less iodinated versions of the thyroid hormone such as T2 which has profound effects on lipid metabolism and insulin sensitivity in hepatocytes, and the modulation of deiodinases that can inactivate thyroid hormones.
The continuum of care of anticancer treatment-induced hypothyroidism in patients with solid non-thyroid tumors: time for an intimate collaboration between oncologists and endocrinologists
Published in Expert Review of Clinical Pharmacology, 2022
Maria V. Deligiorgi, Dimitrios T. Trafalis
Additional future therapeutic perspectives are the development of TH analogs possessing both thyromimetic and antitumor properties with a favorable benefit to risk profile, and the clinical implications of the expanding spectrum of endogenous TH metabolites [40–43].