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巨噬细胞炎性蛋白-1

Macrophage inflammatory protein-1.

作者信息

Menten Patricia, Wuyts Anja, Van Damme Jo

机构信息

Laboratory of Molecular Immunology, Rega Institute for Medical Research, Minderbroedersstraat 10, B-3000, Leuven Belgium.

出版信息

Cytokine Growth Factor Rev. 2002 Dec;13(6):455-81. doi: 10.1016/s1359-6101(02)00045-x.

DOI:10.1016/s1359-6101(02)00045-x
PMID:12401480
Abstract

Macrophage inflammatory protein-1alpha (MIP-1alpha) and MIP-1beta are highly related members of the CC chemokine subfamily. Despite their structural similarities, MIP-1alpha and MIP-1beta show diverging signaling capacities. Depending on the MIP-1 subtype and its NH(2)-terminal processing, one or more of the CC chemokine receptors CCR1, CCR2, CCR3 and CCR5 are recognized. Since both human MIP-1alpha subtypes (LD78alpha and LD78beta) and MIP-1beta signal through CCR5, the major co-receptor for M-tropic HIV-1 strains, these chemokines are capable of inhibiting HIV-1 infection in susceptible cells. In this review, different aspects of human and mouse MIP-1alpha and MIP-1beta are discussed, including their protein and gene structures, their regulated production, their receptor usage and biological activities and their role in several pathologies including HIV-1 infection.

摘要

巨噬细胞炎性蛋白-1α(MIP-1α)和MIP-1β是CC趋化因子亚家族中高度相关的成员。尽管它们在结构上相似,但MIP-1α和MIP-1β显示出不同的信号传导能力。根据MIP-1亚型及其氨基末端加工情况,CC趋化因子受体CCR1、CCR2、CCR3和CCR5中的一个或多个会被识别。由于人类的两种MIP-1α亚型(LD78α和LD78β)以及MIP-1β都通过CCR5信号传导,而CCR5是M型嗜亲性HIV-1毒株的主要共受体,因此这些趋化因子能够抑制HIV-1在易感细胞中的感染。在这篇综述中,将讨论人类和小鼠MIP-1α及MIP-1β的不同方面,包括它们的蛋白质和基因结构、它们的调节性产生、它们的受体使用情况和生物学活性以及它们在包括HIV-1感染在内的几种病理状况中的作用。

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Macrophage inflammatory protein-1.巨噬细胞炎性蛋白-1
Cytokine Growth Factor Rev. 2002 Dec;13(6):455-81. doi: 10.1016/s1359-6101(02)00045-x.
2
Diverging binding capacities of natural LD78beta isoforms of macrophage inflammatory protein-1alpha to the CC chemokine receptors 1, 3 and 5 affect their anti-HIV-1 activity and chemotactic potencies for neutrophils and eosinophils.巨噬细胞炎性蛋白-1α的天然LD78β亚型对CC趋化因子受体1、3和5的不同结合能力影响其抗HIV-1活性以及对嗜中性粒细胞和嗜酸性粒细胞的趋化能力。
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The LD78beta isoform of MIP-1alpha is the most potent CC-chemokine in inhibiting CCR5-dependent human immunodeficiency virus type 1 replication in human macrophages.MIP-1α的LD78β亚型是在抑制人巨噬细胞中CCR5依赖性1型人类免疫缺陷病毒复制方面最有效的CC趋化因子。
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A chimeric MIP-1alpha/RANTES protein demonstrates the use of different regions of the RANTES protein to bind and activate its receptors.一种嵌合的MIP-1α/趋化因子RANTES蛋白展示了利用趋化因子RANTES蛋白的不同区域来结合并激活其受体。
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In vivo evolution of HIV-1 co-receptor usage and sensitivity to chemokine-mediated suppression.HIV-1辅助受体使用情况的体内演变以及对趋化因子介导抑制作用的敏感性。
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MIP-1alpha[CCL3] acting on the CCR1 receptor mediates neutrophil migration in immune inflammation via sequential release of TNF-alpha and LTB4.作用于CCR1受体的MIP-1α[CCL3]通过依次释放肿瘤坏死因子-α(TNF-α)和白三烯B4(LTB4)介导免疫炎症中的中性粒细胞迁移。
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