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. 2022 Sep 30;19(11):1263–1278. doi: 10.1038/s41423-022-00925-7

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© The Author(s), under exclusive licence to CSI and USTC 2022, Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.

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Fig. 8 — Serine metabolism regulates the SAM-IGF1-p38 axis to orchestrate macrophage polarization. Suppressing the serine biosynthesis pathway either by inhibition of PHGDH activity or by exogenous serine and glycine restriction, robustly enhances M(IFN-γ) polarization but suppresses M(IL-4) polarization both in vitro and in vivo. Serine metabolism deficiency increases the expression of IGF1 by reducing the abundance of SAM-dependent H3K27me3 in the promoter of the Igf1 gene. IGF1 then activates the p38-dependent JAK–STAT1 axis to promote M(IFN-γ) polarization and suppress STAT6-mediated M(IL-4) activation