G-CSF: A key regulator of neutrophil production, but that's not all!
G-CSF: A key regulator of neutrophil production, but that's not all!
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DOI：
10.1080/08977190500055836
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发表时间：
2005-03-01
期刊：
影响因子：
1.8
通讯作者：
Roberts, AW
中科院分区：
文献类型：
--
作者：
Roberts, AW
G-CSF 是造血和先天免疫系统的主要细胞外调节剂。 G-CSF 因其在体外半固体培养物中对中性粒细胞祖细胞生长的相对特异性刺激而得名（Burgess 和 Metcalf 1980，Nicola 等人 1983），G-CSF 影响中性粒细胞谱系中从造血干细胞到成熟中性粒细胞的所有细胞的存活、增殖和分化。此外，G-CSF影响成熟中性粒细胞的功能。这些作用支撑了它作为一种药物迅速进入临床医学，增加化疗引起的中性粒细胞减少症患者中性粒细胞的产生。正在进行的研究已经揭示了 G-CSF 最初未被怀疑的多功能性。 G-CSF 被公认为是造血干细胞从骨髓进入血液的有效动员剂，现在越来越多地被认为是免疫反应的调节剂。 G-CSF 的这两种“新”作用首先是通过 G-CSF 临床试验期间的观察发现的。随后对这种多功能性的细胞和分子基础的研究产生了关于 G-CSF 生物学的令人兴奋的新知识。这篇综述强调了有关 G-CSF 信号传导、G-CSF 诱导干细胞动员机制以及 G-CSF 如何影响 T 细胞功能和树突状细胞激活的最新进展。我们试图将当前关于 G-CSF 生物学的问题与其当前和未来的临床应用联系起来。
G-CSF is a major extracellular regulator of haemopoiesis and the innate immune system. Named for its relatively specific stimulation of the growth of neutrophil progenitor cells in vitro in semi-solid cultures (Burgess and Metcalf 1980, Nicola et al. 1983), G-CSF influences the survival, proliferation and differentiation of all cells in the neutrophil lineage, from haemopoietic stem cell through to mature neutrophil. Further, G-CSF influences the function of mature neutrophils. These actions underpin its rapid uptake into clinical medicine as a drug that increases the production of neutrophils in patients with chemotherapy-induced neutropenia.Ongoing research has uncovered initially unsuspected polyfunctionality for G-CSF. G-CSF is well recognised as a potent mobiliser of haemopoietic stem cells from the bone marrow into the blood, and now is being increasingly accepted as a regulator of immune responses. These two "new" actions of G-CSF first came to light through observations made during clinical trials of G-CSF. Subsequent investigations into the cellular and molecular basis for this polyfunctionality have generated exciting new knowledge about the biology of G-CSF. This review emphasises recent advances in knowledge about G-CSF signalling, mechanisms of G-CSF-induced stem cell mobilisation, and how G-CSF influences T-cell function and dendritic cell activation. An attempt is made to link the current issues about the biology of G-CSF with its clinical uses, both present and future.