Klf10 inhibits IL-12p40 production in macrophage colony-stimulating factor-induced mouse bone marrow-derived macrophages.
Klf10 inhibits IL-12p40 production in macrophage colony-stimulating factor-induced mouse bone marrow-derived macrophages.
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DOI：
10.1002/eji.201242697
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发表时间：
2013-01
影响因子：
5.4
通讯作者：
Wang, Lie
中科院分区：
文献类型：
--
作者：
Zhang, Wei;Wang, Xuelian;Xia, Xiaoping;Liu, Xia;Suo, Shanshan;Guo, Jing;Li, Min;Cao, Wenqiang;Cai, Zhijian;Hui, Zhaoyuan;Subramaniam, Malayannan;Spelsberg, Thomas C.;Wang, Jianli;Wang, Lie
用粒细胞-巨噬细胞集落刺激因子（GM-CSF）或巨噬细胞集落刺激因子（M-CSF）处理的骨髓源性巨噬细胞（BMMs）分化为GM-CSF诱导的小鼠骨髓源性巨噬细胞（GM-BMMs）或M-CSF诱导的小鼠骨髓源性巨噬细胞（M-BMMs），它们分别具有M1或M2特征。GM-β-内酰胺酶产生大量促炎细胞因子并介导对病原体的抵抗，而M-β-内酰胺酶产生有助于组织修复和重塑的抗炎细胞因子。脂多糖（LPS）刺激的M-β细胞处于IL-12低IL-10高表型，即IL-12低IL-10高表型。然而，这一过程的监管仍不清楚。Klf 10属于Krüppel样转录因子家族，最初被描述为TGF-β诱导的早期基因1。IL-12 p40在Klf 10缺陷小鼠的LPS刺激的M-Bcl 3中上调，但在Klf 10过表达期间下调。Klf 11是Krüppel样因子家族的另一个成员，也可以抑制IL-12 p40的产生。此外，Klf 10结合IL-12 p40启动子的CACCC元件并抑制其转录。因此，我们已将Klf 10鉴定为调节M-BMMs中IL-12 p40表达的转录因子。
Bone marrow-derived macrophages (BMMs) treated with granulocyte-macrophage colony-stimulating factor (GM-CSF) or macrophage colony-stimulating factor (M-CSF), differentiate into GM-CSF-induced mouse bone marrow-derived macrophages (GM-BMMs) or M-CSF-induced mouse bone marrow-derived macrophages (M-BMMs), which have an M1 or M2 profile, respectively. GM-BMMs produce large amounts of proinflammatory cytokines and mediate resistance to pathogens, whereas M-BMMs produce anti-inflammatory cytokines that contribute to tissue repair and remodeling. M-BMMs stimulated with lipopolysaccharide (LPS) are in an antiinflammatory state, with an IL-12low IL-10high phenotype. However, the regulation of this process remains unclear. Klf10 belongs to the family of Krüppel-like transcription factors and was initially described as a TGF-β inducible early gene 1. IL-12p40 is upregulated in LPS-stimulated M-BMMs from Klf10-deficient mice, but downregulated during Klf10 overexpression. Klf11, another member of the Krüppel-like factor family, can also repress the production of IL-12p40. Furthermore, Klf10 binds to the CACCC element of the IL-12p40 promoter and inhibits its transcription. We have therefore identified Klf10 as a transcription factor that regulates the expression of IL-12p40 in M-BMMs.
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