Research Article

Anti-inflammatory effect of IL-10 mediated by metabolic reprogramming of macrophages

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Science  05 May 2017:
Vol. 356, Issue 6337, pp. 513-519
DOI: 10.1126/science.aal3535

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A way to switch off IBD

Inflammatory bowel diseases (IBDs) such as ulcerative colitis and Crohn's disease are associated with defective interleukin-10 (IL-10) signaling. Although IL-10 plays an essential role in the control and resolution of inflammation, the mechanisms responsible for its anti-inflammatory actions remain unclear. Ip et al. show that in response to inflammation, IL-10 controls cellular metabolism in macrophages by inducing the mTOR inhibitor DDIT4 and preventing glucose uptake (see the Perspective by Kabat and Pearce). In mouse models and patient samples, defective IL-10 promoted accumulation of damaged macrophages and exacerbated inflammatory signals. Targeting mTORC1 thus might help to treat IBD and related disorders.

Science, this issue p. 513; see also p. 488

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