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. Author manuscript; available in PMC: 2016 Aug 10.
Published in final edited form as: Lancet Diabetes Endocrinol. 2015 Jun 10;3(10):816–825. doi: 10.1016/S2213-8587(15)00225-9

Figure 1. Schematic representation of hypothalamic thyroid hormone signalling during inflammation.

Figure 1

Inflammation activates the NFκB pathway in tanycytes, specialised cells lining the third ventricle. Tanycytes express D2, the main T3 producing enzyme in the brain, the promoter of which contains NFκB responsive elements. Binding of NFκB increases D2 expression and activity, and this stimulates the conversion of T4 into T3. T3 will enter adjacent neurons and bind to neuronal TRβ thereby regulating transcriptional activity of TRH. T3=tri-iodothyronine. TRβ=thyroid hormone receptor β. TRH=thyrotropin-releasing hormone. NFκB=nuclear factor kappa-light-chain-enhancer of activated B cells. D2=deiodinase type 2. T4=thyroxine.