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GM-CSF:从生长因子到组织炎症的中枢介质。

GM-CSF: From Growth Factor to Central Mediator of Tissue Inflammation.

机构信息

Institute of Experimental Immunology, University of Zurich Winterthurerstrasse 190, 8057 Zurich, Switzerland.

Institute of Experimental Immunology, University of Zurich Winterthurerstrasse 190, 8057 Zurich, Switzerland.

出版信息

Immunity. 2016 Nov 15;45(5):963-973. doi: 10.1016/j.immuni.2016.10.026.

DOI:10.1016/j.immuni.2016.10.026
PMID:27851925
Abstract

The granulocyte-macrophage colony-stimulating factor (GM-CSF) was initially classified as a hematopoietic growth factor. However, unlike its close relatives macrophage CSF (M-CSF) and granulocyte CSF (G-CSF), the majority of myeloid cells do not require GM-CSF for steady-state myelopoiesis. Instead, in inflammation, GM-CSF serves as a communication conduit between tissue-invading lymphocytes and myeloid cells. Even though lymphocytes are in all likelihood the instigators of chronic inflammatory disease, GM-CSF-activated phagocytes are well equipped to cause tissue damage. The pivotal role of GM-CSF at the T cell:myeloid cell interface might shift our attention toward studying the function of the myeloid compartment in immunopathology. Targeting specifically the crosstalk between T cells and myeloid cells through GM-CSF holds promise for the development of therapeutics to combat chronic tissue inflammation. Here, we will review some of the major discoveries of the recent past, which indicate that GM-CSF is so much more than its name suggests.

摘要

粒细胞-巨噬细胞集落刺激因子 (GM-CSF) 最初被归类为造血生长因子。然而,与它的近亲巨噬细胞集落刺激因子 (M-CSF) 和粒细胞集落刺激因子 (G-CSF) 不同,大多数髓系细胞在稳态造血过程中并不需要 GM-CSF。相反,在炎症中,GM-CSF 充当浸润淋巴细胞和髓系细胞之间的通讯渠道。尽管淋巴细胞很可能是慢性炎症性疾病的始作俑者,但 GM-CSF 激活的吞噬细胞完全有能力造成组织损伤。GM-CSF 在 T 细胞:髓系细胞界面的关键作用可能会促使我们关注研究髓系细胞在免疫病理学中的功能。通过 GM-CSF 特异性靶向 T 细胞和髓系细胞之间的串扰,为开发治疗慢性组织炎症的疗法带来了希望。在这里,我们将回顾过去的一些重大发现,这些发现表明 GM-CSF 的作用远不止其名称所暗示的那样。

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