Role of macrophage inflammatory protein (MIP)-1α/CCL3 in leukemogenesis.
Role of macrophage inflammatory protein (MIP)-1α/CCL3 in leukemogenesis.
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DOI：
10.4161/mco.29899
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发表时间：
2014
影响因子：
2.1
通讯作者：
Mukaida N
中科院分区：
文献类型：
--
作者：
Baba T;Mukaida N
CC趋化因子巨噬细胞炎性蛋白-1α(α-1 MIP-1/CCL3)自首次被鉴定为巨噬细胞源性炎症介质以来，其生物学功能已被广泛研究。除了其致炎活性外，CCL3还负向调节造血干/祖细胞(HSPC)的增殖。基于这一独特的功能，CCL3也被称为干细胞抑制物。这一特性促使许多研究人员研究CCL3对正常生理性造血和血液系统恶性肿瘤的病理生理过程的影响。因此，有越来越多的证据支持CCL3在几种类型的白血病的病理生理学中的关键参与，这些白血病是由HSPC的肿瘤转化引起的。在这篇综述中，我们讨论了CCL3在白血病发生中的作用，以及它作为一种新的白血病治疗策略的靶点的潜在价值。
The biologic function of the CC chemokine macrophage inflammatory protein-1α (MIP-1α/CCL3) has been extensively studied since its initial identification as a macrophage-derived inflammatory mediator. In addition to its proinflammatory activities, CCL3 negatively regulates the proliferation of hematopoietic stem/progenitor cells (HSPCs). On the basis of this unique function, CCL3 is alternatively referred to as a stem cell inhibitor. This property has prompted many researchers to investigate the effects of CCL3 on normal physiologic hematopoiesis and pathophysiologic processes of hematopoietic malignancies. Consequently, there is accumulating evidence supporting a crucial involvement of CCL3 in the pathophysiology of several types of leukemia arising from neoplastic transformation of HSPCs. In this review we discuss the roles of CCL3 in leukemogenesis and its potential value as a target in a novel therapeutic strategy for the treatment of leukemia.