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serine metabolism orchestrates macrophage polarization by regulating the IGF1–p38 axis

Cellular & Molecular Immunology 2022年第11期19卷 1263-1278页

作者： Xiao Shan Penghui Hu Lina Ni Long Shen Yanan Zhang Zemin Ji Yan Cui Meihua Guo Haoan Wang Liyuan Ran Kun Yang Ting Wang Lei Wang Bin Chen Zhi Yao Vingjie Wu Qiujing Yu Tianjin Institute of Immunology Key Laboratory of Immune Microenvironment and Disease of the Ministry of EducationThe Province and Ministry Co-sponsored Collaborative Innovation Center for Medical EpigeneticsTianjin Key Laboratory of Inflammation BiologyDepartment of ImmunologySchool of Basic Medical SciencesTianjin Medical University Division of Infectious Disease Second Hospital of Tianjin Medical UniversityTianjin300070China Institute for Genome Engineered Animal Models of Human Diseases National Center of Genetically Engineered Animal Models for International ResearchDalian Medical UniversityDalian116044LiaoningChina Shandong Provincial Hospital School of Laboratory Animal and Shandong Laboratory Animal CenterScience and Technology Innovation CenterShandong First Medical University and Shandong Academy of Medical SciencesJinan250021ShandongChina The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics Department of Pharmacology and Tianjin Key Laboratory of Inflammation BiologySchool of Basic Medical SciencesTianjin Medical UniversityTianjin300070China Tianjin Institute of Immunology Key Laboratory of Immune Microenvironment and Disease of the Ministry of EducationDepartment of ImmunologySchool of Basic Medical SciencesTianjin Medical UniversityTianjinChina Department of Molecular Pathobiology New York University College of DentistryNew YorkNY10010USA

serine metabolism is reportedly involved in immune cell functions, but whether and how serine metabolism regulates macrophage polarization remain largely unknown. Here, we show that suppressing serine metabolism, either by inhibiting the activity of the key enzyme phosphoglycerate dehydrogenase in the serine biosynthesis pathway or by exogenous serine and glycine restriction, robustly enhances the polarization of interferon-γ-activated macrophages (M(IFN-γ)) but suppresses that of interleukin-4-activated macrophages (M(IL-4)) both in vitro and in vivo. Mechanistically, serine metabolism deficiency increases the expression of IGF1 by reducing the promoter abundance of S-adenosyl methionine-dependent histone H3 lysine 27 trimethylation. IGF1 then activates the p38-dependent JAK–STAT1 axis to promote M(IFN-γ) polarization and suppress STAT6-mediated M(IL-4) activation. This study reveals a new mechanism by which serine metabolism orchestrates macrophage polarization and suggests the manipulation of serine metabolism as a therapeutic strategy for macrophage-mediated immune diseases.

关键词： serine metabolism PHGDH Macrophage polarization SAM IGF1 p38

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