Triiodothyronine antibody was raised in mouse using triiodothyronine (T3)-BSA as the immunogen.
Conjugate
Unconjugated
Target
Alternative Names
Triiodothyronine; T3
Citations
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Background
Early in the last century, researchers identified monoiodotyrosine and diiodotyrosine, thyroxine (T4), and iodide in thyroid extracts, and found an unknown substance in them. First, they demonstrated the presence of the unknown substance in the plasma of humans treated with 131I, then they synthesized 3,5,3'-triiodothyronine (T3) from 3,5-diiodothyronine and demonstrated that the previously discovered unknown substance was chromatographically indistinguishable from synthetic T3, finally they isolated T3 from bovine thyroid tissue and demonstrated that its X-ray crystallographic characteristics were identical to those of synthetic T3. The researchers then found that when T3 was given to hypothyroid patients, their basal metabolic rate and plasma cholesterol levels returned to normal. In the rat goiter prevention test, T3 was three times more potent than T4. They therefore concluded that T3 is the active form of thyroid hormone (TH), produced by T4.
Figure 1. Chemical structure of triiodothyronine (Source: Paz S, et al. 2018)
Most T4 and T3 are tightly bound to carrier proteins in the bloodstream and are not directly taken up by cells. Only a small fraction of unbound free T4 and T3 molecules can enter tissues and cells through specific transporters to form an intracellular pool of TH. It is estimated that about 2/3 of T3 is present in the tissues, while 2/3 of T4 remains in the plasma. T3 levels in the plasma region are in balance with those in the tissue region, and any change in plasma T3 levels directly affects T3 levels in the tissues. Some tissues express deiodinase, which converts T4 to T3 and thus affects tissue T3 levels, although the phenomenon is not related to plasma TH levels.
Changes in T3 levels in tissues are of clinical value and will reflect the physiopathological state of the organism. Researchers are currently working to explore clinically relevant tissue-specific biomarkers that reflect the role of T3. Serum TSH reflects plasma T4 and T3 levels and is the best biomarker to suggest the role of T3 in the medial hypothalamic basal lamina and pituitary gland. In addition, there are a number of biomarkers that reflect the role of T3 that exhibit some tissue specificity but lack sensitivity. For example, basal metabolic rate reflects the role of T3 in metabolism-related tissues, and serum cholesterol reflects the role of T3 in the liver.
Alternative Names
Anti-T3 monoclonal antibody
References
1. Paz S, et al. Iodine: An Essential Trace Element. Med J Clin Trials Case Stud. 2018 Aug;2(8).
2. Morris JC, et al. The isolation of thyroxine (T4), the discovery of 3,5,3'-triiodothyronine (T3), and the identification of the deiodinases that generate T3 from T4: An historical review. Endocrine. 2019 Oct;66(1):3-9.
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References
Triiodothyronine induces a proinflammatory monocyte/macrophage profile and impedes cardiac regeneration
J Mol Cell Cardiol
Authors: Chen Z, Cai D, Xie Y, Zhong J, Wu M, Yang H, Feng J, Lian H, Dou K, Nie Y.
Neonatal mouse hearts can regenerate post-injury, unlike adult hearts that form fibrotic scars. The mechanism of thyroid hormone signaling in cardiac regeneration warrants further study. We found that triiodothyronine impairs cardiomyocyte proliferation and heart regeneration in neonatal mice after apical resection. Single-cell RNA-Sequencing on cardiac CD45-positive leukocytes revealed a pro-inflammatory phenotype in monocytes/macrophages after triiodothyronine treatment. Furthermore, we observed that cardiomyocyte proliferation was inhibited by medium from triiodothyronine-treated macrophages, while triiodothyronine itself had no direct effect on the cardiomyocytes in vitro. Our study unveils a novel role of triiodothyronine in mediating the inflammatory response that hinders heart regeneration.
Limited Utility of Free Triiodothyronine Testing
J Appl Lab Med
Authors: Lin Y, Riek AE, Gronowski AM, Farnsworth CW.
Background: Free triiodothyronine (fT3) testing is most useful when thyroid stimulating hormone (TSH) is suppressed, and free thyroxine (fT4) is normal or decreased. These laboratory values in a symptomatic patient are referred to as T3 thyrotoxicosis. Standards for fT3 reflex testing have not been established. Herein, we examined the clinical utility of fT3 with the goal of identifying a TSH cutoff in the context of normal/decreased fT4 that maximizes the utility of measuring fT3.
Methods: TSH, fT4, and fT3 results between January 2016 and October 2021 were extracted from the laboratory information system and grouped if resulted on the same day for the same patient. Frequency of biochemical T3 thyrotoxicosis was evaluated at different TSH cutoffs and in outpatient vs inpatient settings.
Results: Of the 4366 TSH-fT4-fT3 results, 70 (1.6%) were consistent with biochemical T3 thyrotoxicosis. The common reasons were previously diagnosed hyperthyroidism on antithyroid medication (n = 28) or hypothyroidism on thyroid medication (n = 18) and newly diagnosed hyperthyroidism (n = 20, 0.5%). The likelihood of detecting T3 thyrotoxicosis increased with lower TSH cutoff (<0.3 μIU/mL, 10.3% vs <0.0 1μIU/mL, 27.6%). All patients with newly diagnosed hyperthyroidism had TSH <0.01 μIU/mL. Higher frequency of T3 thyrotoxicosis was observed in the outpatient setting (34%) relative to the inpatient setting (14%, P < 0.001) when TSH < 0.01 μIU/mL.
Conclusions: T3 thyrotoxicosis is a relatively rare diagnosis and fT3 measurement has limited utility in the vast majority of patients. A fT3 reflex for patients with TSH <0.01 μIU/mL and normal/low fT4 may improve clinical utility and reduce unnecessary testing, especially in the outpatient setting.
COA
Publication 
Figure 1. Chemical structure of triiodothyronine
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