Volume 68 | February 2023

Cover Story

In ‘classic’ polarisation, macrophages undergo pro-inflammatory M1 activation in response to cues including Toll Like Receptor (TLR) agonists and IFNγ but in contrast, in response to agents including IL-4, IL-10 or IL-13, they become M2 macrophages, which are generally thought of as having anti-inflammatory or tissue repair actions. Aberrant regulation of macrophage polarisation and activation is suspected to underlie pathology in metabolic illness such as diabetes and cardiovascular disease but the regulatory paradigms underlying immunometabolic control are still being determined. During an early evolutionary phase, regulation of immunometabolic enzymes is likely to have occurred in response to nutrients and metabolites such as itaconate, which has been shown to mediate suppression of M1 cytokines, IL-1β and TNF-α, as well as suppression of the M1 marker iNOS.

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