OK, OK - so Deiodinase Type 3 is essential for the functioning of neutrophils. But WHY?
[Many years ago, I remember reading the idea that in certain circumstances thyroid hormone(s) would be deiodinated in order to release iodine atoms - with the iodine then being available to kill bacteria (or whatever). Seemed a neat idea but rather too fanciful. However, the marked increase in thyroxine and reverse-T3 reported here is interesting. More T4 to deliver more iodine, but deiodinated - and releasing that iodine atom - to rT3 so as to avoid increasing T3? Surely not? Feel free to tell me what an idiotic idea this is. 
]
Endocrinology. 2018 Feb 1;159(2):826-835. doi: 10.1210/en.2017-00666.
The Thyroid Hormone Inactivating Type 3 Deiodinase Is Essential for Optimal Neutrophil Function: Observations From Three Species.
van der Spek AH1, Jim KK2,3, Karaczyn A4, van Beeren HC1, Ackermans MT5, Darras VM6, Vandenbroucke-Grauls CMJE3, Hernandez A4, Brouwer MC2, Fliers E1, van de Beek D2, Boelen A1.
Author information
1 Department of Endocrinology and Metabolism, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
2 Department of Neurology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
3 Department of Medical Microbiology and Infection Control, VU University Medical Center, Amsterdam, the Netherlands.
4 Center for Molecular Medicine, Maine Medical Center Research Institute, Scarborough, Maine.
5 Laboratory of Endocrinology, Department of Clinical Chemistry, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
6 Laboratory of Comparative Endocrinology, Department of Biology, KU Leuven, Leuven, Belgium.
Abstract
Neutrophils are essential effector cells of the innate immune system that have recently been recognized as thyroid hormone (TH) target cells. Cellular TH bioavailability is regulated by the deiodinase enzymes, which can activate or inactivate TH. We have previously shown that the TH inactivating enzyme type 3 deiodinase (D3) is present in neutrophils. Furthermore, D3 knockout (D3KO) mice show impaired bacterial killing upon infection. We hypothesized that D3 plays a role in neutrophil function during infection by actively regulating local TH availability. We measured TH concentrations in cerebrospinal fluid (CSF) from patients with bacterial meningitis and controls. Bacterial meningitis resulted in marked changes in CSF TH levels, characterized by a strong increase of thyroxine and reverse-triiodothyronine concentrations. This altered TH profile was consistent with elevated D3 activity in infiltrating neutrophils at the site of infection. D3 knockdown in zebrafish embryos with pneumococcal meningitis resulted in increased mortality and reduced neutrophil infiltration during infection. Finally, stimulated neutrophils from female D3KO mice exhibited impaired NADPH-oxidase activity, an important component of the neutrophil bacterial killing machinery. These consistent findings across experimental models strongly support a critical role for reduced intracellular TH concentrations in neutrophil function during infection, for which the TH inactivating enzyme D3 appears essential.
PMID: 29186449
PMCID: PMC5774253 [Available on 2019-02-01]
DOI: 10.1210/en.2017-00666
Free access to full paper will be available - eventually - on 01/02/2019 - for now, just the abstract:
