Abstract

The field that links immunity and metabolism is rapidly expanding. Apparently non-immunological disorders such as obesity and type 2 diabetes have been linked to immune dysregulation suggesting that metabolic alterations can be induced by or be consequence of an altered self-immune tolerance. In this context, a key role is played by signalling systems acting as metabolic “sensors” linking energy/nutritional status to regulatory T (Treg) cell functions such s the adipose tissue derived hormone, leptin. We propose that a dynamic/oscillatory activity of intracellular metabolism might represent a shift in understanding the molecular mechanisms governing Treg cell tolerance. In particular, the decision between Treg cell proliferation and hyporesponsiveness arises from their ability to probe the extracellular milieu and, modulating the metabolic intracellular signalling, to determine different qualitative and quantitative functional outcomes.

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