促炎细胞因子
细胞生物学
生物
STAT6
炎症
巨噬细胞极化
转录因子
表型
化学
免疫学
白细胞介素4
细胞因子
生物化学
基因
作者
Xia Wang,Yindong Ji,Ping Feng,Rucheng Liu,Guosheng Li,Junjie Zheng,Yaqiang Xue,Yaxun Wei,Chunyan Ji,Fan Chen,Jingxin Li
标识
DOI:10.1002/advs.202100209
摘要
Abstract Phenotypic polarization of macrophages is regulated by a milieu of cues in the local tissue microenvironment. Currently, little is known about how the intrinsic regulators modulate proinflammatory (M1) versus prohealing (M2) macrophages activation. Here, it is observed that insulin‐like growth factor 2 messenger RNA (mRNA)‐binding protein 2 (IGF2BP2)‐deleted macrophages exhibit enhanced M1 phenotype and promote dextran sulfate sodium induced colitis development. However, the IGF2BP2 −/− macrophages are refractory to interleukin‐4 (IL‐4) induced activation and alleviate cockroach extract induced pulmonary allergic inflammation. Molecular studies indicate that IGF2BP2 switches M1 macrophages to M2 activation by targeting tuberous sclerosis 1 via an N6‐methyladenosine (m 6 A)‐dependent manner. Additionally, it is also shown a signal transducer and activators of transcription 6 (STAT6)‐high mobility group AT‐hook 2‐IGF2BP2‐peroxisome proliferator activated receptor‐ γ axis involves in M2 macrophages differentiation. These findings highlight a key role of IGF2BP2 in regulation of macrophages activation and imply a potential therapeutic target of macrophages in the inflammatory diseases.
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