Role of TLR6 in controlling macrophage iron accumulation

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Beschreibung der Arbeit

Molecular and cellular assays will be performed in primary macrophages isolated from TLR6-deficient and wild-type mice.

Iron export via ferroportin (FPN) is essential for iron transport to the plasma. Iron accumulation in macrophages acts as a check point for pro-inflammatory reprogramming. We recently identified mechanisms how ferroportin is controlled by transcriptional repression and protein degradation via the hormone Hepcidin. TLR6 is a transmembrane protein that belongs to the pattern recognition receptor family that plays an important role during infections. Evidence for TLR6 functions under steady state conditions are rarely reported. Our analysis of Toll-like receptor (TLR) 6 deficient mice demonstrates that TLR6-deficiency suppresses FPN protein levels under steady state levels (e.g. in the absence of inflammation). As a consequence, iron levels are increased in macrophages of the spleen. In this project, we aim to gain mechanistic insight into how TLR6 acts as a checkpoint of iron export to trigger intracellular iron accumulation in macrophages.

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Vollzeit Forschung

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