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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >Functional overlap but differential expression of CSF-1 and IL-34 in their CSF-1 receptor-mediated regulation of myeloid cells
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Functional overlap but differential expression of CSF-1 and IL-34 in their CSF-1 receptor-mediated regulation of myeloid cells

机译：CSF-1和IL-34在CSF-1受体介导的髓样细胞调节中的功能重叠但差异表达

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CSF-1 is broadly expressed and regulates macrophage and osteoclast development. The action and expression of IL-34, a novel CSF-1R ligand, were investigated in the mouse. As expected, huIL-34 stimulated macrophage proliferation via the huCSF-1R, equivalently to huCSF-1, but was much less active at stimulating mouse macrophage proliferation than huCSF-1. Like muCSF-1, muIL-34 and a muIL-34 isoform lacking Q81 stimulated mouse macrophage proliferation, CSF-1R tyrosine phosphorylation, and signaling and synergized with other cytokines to generate macrophages and osteoclasts from cultured progenitors. However, they respectively possessed twofold and fivefold lower affinities for the CSF-1R and correspondingly, lower activities than muCSF-1. Furthermore, muIL-34, when transgenically expressed in a CSF-1-dependent manner in vivo, rescued the bone, osteoclast, tissue macrophage, and fertility defects of Csf1op/op mice, suggesting similar regulation of CSF-1R-expressing cells by IL-34 and CSF-1. Whole-mount IL34 in situ hybridization and CSF-1 reporter expression revealed that IL34 mRNA was strongly expressed in the embryonic brain at E11.5, prior to the expression of Csf1 mRNA. QRT-PCR revealed that compared with Csf1 mRNA, IL34 mRNA levels were lower in pregnant uterus and in cultured osteoblasts, higher in most regions of the brain and heart, and not compensatorily increased in Csf1op/op mouse tissues. Thus, the different spatiotemporal expression of IL-34 and CSF-1 allows for complementary activation of the CSF-1R in developing and adult tissues.
机译：CSF-1被广泛表达并调节巨噬细胞和破骨细胞的发育。在小鼠中研究了新型CSF-1R配体IL-34的作用和表达。如预期的那样，huIL-34通过huCSF-1R刺激了巨噬细胞的增殖，与huCSF-1相当，但在刺激小鼠巨噬细胞增殖方面的活性远低于huCSF-1。像muCSF-1一样，缺少Q81的muIL-34和muIL-34同工型也能刺激小鼠巨噬细胞增殖，CSF-1R酪氨酸磷酸化，并信号传导并与其他细胞因子协同作用，从而从培养的祖细胞中产生巨噬细胞和破骨细胞。但是，它们对CSF-1R的亲和力分别低2倍和5倍，活性也比muCSF-1低。此外，当在体内以CSF-1依赖性方式转基因表达muIL-34时，可以挽救Csf1op / op小鼠的骨骼，破骨细胞，组织巨噬细胞和生育能力缺陷，这表明IL对CSF-1R表达细胞的调控相似-34和CSF-1。完整的IL34原位杂交和CSF-1报告基因表达表明，在表达Csf1 mRNA之前，IL34 mRNA在E11.5的胚胎脑中强烈表达。 QRT-PCR显示，与Csf1 mRNA相比，孕妇子宫和培养的成骨细胞中IL34 mRNA的水平较低，在大脑和心脏的大多数区域较高，并且在Csf1op / op小鼠组织中没有补偿性的升高。因此，IL-34和CSF-1的时空表达不同，可以在发育和成人组织中互补激活CSF-1R。

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