Modulation of M2 macrophage polarization by the crosstalk between Stat6 and Trim24

Tao Yu(Shanghai Jiao Tong University), Shucheng Gan(Shanghai Jiao Tong University), Qingchen Zhu(Shanghai Jiao Tong University), Dongfang Dai(Jiangsu University), Ni Li(Shanghai Jiao Tong University), Hui Wang(Ruijin Hospital), Xiaosong Chen(Ruijin Hospital), Dan Hou(Shanghai Jiao Tong University), Yan Wang(Shanghai Jiao Tong University), Qiang Pan‐Hammarström(Shanghai Jiao Tong University), Jing Xu(Shanghai Jiao Tong University), Xingli Zhang(Shanghai Jiao Tong University), Junli Liu(Shanghai Jiao Tong University), Siyu Pei(Shanghai Jiao Tong University), Chao Peng, Ping Wu, Simona Romano(University of Naples Federico II), Chaoming Mao(Jiangsu University), Mingzhu Huang(Fudan University Shanghai Cancer Center), Xiaodong Zhu(Fudan University Shanghai Cancer Center), Kunwei Shen(Ruijin Hospital), Jun Qin(Chinese Academy of Sciences), Yichuan Xiao(Shanghai Jiao Tong University)
Nature Communications
September 25, 2019
Cited by 342Open Access
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Abstract

Stat6 is known to drive macrophage M2 polarization. However, how macrophage polarization is fine-tuned by Stat6 is poorly understood. Here, we find that Lys383 of Stat6 is acetylated by the acetyltransferase CREB-binding protein (CBP) during macrophage activation to suppress macrophage M2 polarization. Mechanistically, Trim24, a CBP-associated E3 ligase, promotes Stat6 acetylation by catalyzing CBP ubiquitination at Lys119 to facilitate the recruitment of CBP to Stat6. Loss of Trim24 inhibits Stat6 acetylation and thus promotes M2 polarization in both mouse and human macrophages, potentially compromising antitumor immune responses. By contrast, Stat6 mediates the suppression of TRIM24 expression in M2 macrophages to contribute to the induction of an immunosuppressive tumor niche. Taken together, our findings establish Stat6 acetylation as an essential negative regulatory mechanism that curtails macrophage M2 polarization.


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