Role of CXCR4 chemokine receptor blockade using AMD3100 for mobilization of autologous hematopoietic progenitor cells
Role of CXCR4 chemokine receptor blockade using AMD3100 for mobilization of autologous hematopoietic progenitor cells
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DOI：
10.1159/000088410
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发表时间：
2005-01-01
影响因子：
2.4
通讯作者：
Calandra, G
中科院分区：
文献类型：
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作者：
Flomenberg, N;DiPersio, J;Calandra, G
G-CSF动员造血祖细胞(HPC)是通过成熟的髓系细胞释放酶，导致黏附分子、营养趋化因子及其受体和细胞外基质的消化。通过趋化因子SDF-1α/CXCL12与其受体CXCR4结合的营养效应，HPC进入并保留在骨髓中。AMD3100可逆地抑制SDF-1α/CXCR4结合，AMD3100可动员CD34+细胞进入循环。AMD3100已经在几个临床试验中进行了测试，这些试验表明，它可以改善动员的CD34+细胞的数量，包括无法单独使用G-CSF动员的患者。AMD3100动员的细胞植入迅速和持久。毒性是温和的，而且很少发生。淋巴瘤和骨髓瘤细胞似乎没有被动员起来。AMD3100似乎是一种很有前途的HPC动员试剂。版权所有(C)2005年S.Karger AG，巴塞尔。
G-CSF mobilization of hematopoietic progenitor cells (HPCs) is mediated through enzyme release from maturing myeloid cells, leading to digestion of adhesion molecules, trophic chemokines and their receptors, and the extracellular matrix. HPCs traffic to and are retained in the marrow through the trophic effects of the chemokine SDF-1 alpha/CXCL12 binding to its receptor, CXCR4. AMD3100 reversibly inhibits SDF-1 alpha/CXCR4 binding, and AMD3100 administration mobilizes CD34+ cells into the circulation. AMD3100 has been tested in several clinical trials which demonstrate that it improves the number of CD34+ cells mobilized including patients failing to mobilize with G-CSF alone. Engraftment of AMD3100-mobilized cells is prompt and durable. Toxicities are mild and infrequent. Lymphoma and myeloma cells do not appear to be mobilized. AMD3100 appears to be a promising agent for HPC mobilization. Copyright (c) 2005 S. Karger AG, Basel.