This is (so far in preprint form so not generally available) a paper which shows how our cells are controlled by deiodinase enzymes. The answer is quite clear: The deiodinase called D2 is stimulated by T3 using one activator, whereas deiodinase D3 is inhibited by T3 using a deactivator. The latter is the one that makes rT3 from T4. So the expression of the right amount of T3 in each cell depends on the balance between D2 and D3 action, which pull opposite ways. This accounts not only for the unique expression in a particular tissue or organ, but the balance between each action can vary from moment to moment according to individual tissue need. So the way individual tissues respond to T4 (competing T3 or rT3 production) explains completely how individual tissues and organs act both in the long term and the short.
A very important paper. I don't know the journal yet as it was sent to me by certain channels . When it is finally accepted I'll send on to TUK or show the doi number if possible to download free
DEIODINASES AND THE METABOLIC CODE FOR THYROID HORMONE ACTION
Samuel C. Russo , Federico Salas-Lucia , and Antonio C. Bianco
Which form of Hrt works well with thyroid replacement hormones. 
how is Armour Thyroid working these days...?
Thyroid hormones test
It's in this journal academic.oup.com/endo/advan... but behind a paywall.
Have you got your introductory comments the wrong way around? Should it say D2 is inhibited by T3 and D3 is stimulated by T3?
A further mechanism that is often ignored is that TSH stimulates D2. So if the axis is down-regulated, or TSH has low bioactivity, there is reduced D2 and hence hypothyroidism is D2 expresssing tissues - even if serum fT3 is normal or rendered normal by tablets.
I think I got it right: D2 enhances activity for T3 p production according to need for extra energy, whereas D3 slows things down and rT3 is preferentially made instead This is the actual abstract:
ABSTRACT
Deiodinases modify the biological activity of thyroid hormone (TH) molecules, i.e. they may activate thyroxine (T4) to 3,5,3’-tri-iodothyronine (T3), or inactivate T3 to 3,3’diiodo-L-thyronine (T2) or T4 to reverse tri-iodothyronine (rT3). Although evidence of deiodination of T4 to T3 was available since the 1950s, objective evidence of TH metabolism was not established until the 1970s. The modern paradigm considers that the deiodinases not only play a role in the homeostasis of circulating T3, but they also provide dynamic control of TH signaling: cells that express the activating type 2 deiodinase (D2) have enhanced TH signaling due to intracellular build-up of T3; the opposite is seen in cells that express type 3 deiodinase (D3), the inactivating deiodinase. D2 and D3 are expressed in metabolically relevant tissues such as brown adipose tissue, skeletal muscle and liver, and their roles have been investigated using cell, animal, and human models. During development, D2 and D3 expression customize for each tissue/organ the timing and intensity of TH signaling. In adult cells, D2 is induced by cyclic adenosine monophosphate (cAMP) and its expression is invariably associated with enhanced T3 signaling, expression of PGC1 and accelerated energy expenditure. In contrast, D3 expression is induced by hypoxia-inducible factor 1- α (HIF-1a), dampening T3 signaling and the metabolic rate. The coordinated expression of these enzymes adjusts TH signaling on a time- and tissue-specific fashion, affecting metabolic pathways in health and disease states.
I was thinking of this sentence "The deiodinase called D2 is stimulated by T3 using one activator, whereas deiodinase D3 is inhibited by T3 using a deactivator. ". I don't know about the activator / deactivator until we see the paper but it seems to say T3 promotes D2 and inhibits D3 whereas T3 promotes D3 and inhibits D2 thus helping to maintain steady intracellular T3 levels.
That is so, but not by changing D2 or D3 levels, but changing the levels of factors that stimulate D2 and otherwise stimulate D3. It is the different stimulants or inhibitors that are key to how the two enzymes react.
OK I'll wait for the full paper. This illustrates the importance of studying the full paper.