ccr5

Some people were born without CCR5 gene , thus having natural immunity against AIDS .

有些人天生就不具有CCR5基因，他们对艾滋病有天然的免疫力。

This variability means that a small deletion on the CCR5 gene .

这种变异是指CCR5基因上一小段缺失。

Conclusion Condyloma acuminata are not associated with genetic polymorphism of CCR5 △ 32 gene .

结论CCR5△32基因多态性与尖锐湿疣无相关性。

Her team used the CCR5 gene from human stem cells , which normally allows the HIV virus to enter human cells .

她的研究组利用了来自人类干细胞的CCR5基因，该基因在正常情况下能让艾滋病病毒进入人类细胞。

ABSTRACT : Objective To investigate the relationship between CCR5 △ 32 gene polymorphism and condyloma acuminata .

摘要：目的探讨CCR5△32基因多态性与尖锐湿疣的关系。

Mesenchymal stem cells promote the migration and proliferation of Saos-2 cells through CCL5 / CCR5 axis

间充质干细胞通过CCL5/CCR5信号途径促进骨肉瘤Saos-2细胞迁移和生长

The team that conducted the study had previously transplanted edited CCR5 human cells into mice , making them resistant to HIV .

进行这项研究的团队此前曾将CCR5编辑过的人类细胞移植到小鼠体内，使其对艾滋病毒具有抵抗力。

Without CCR5 for the HIV to rob , the patient 's immune cells can effectively resist HIV and prevent infection .

如果没有CCR5对艾滋病毒的“抢劫”，病人的免疫细胞能有效地抵抗艾滋病毒并防止其感染发生。

They say morphine blocked HIV from binding to CCR5 receptors it typically uses to enter and infect cells .

他们说，吗啡通过阻止HIV病毒与CCR5的受体的结合阻止了HIV感染，HIV病毒多通过CCR5的受体进入和感染细胞。

Apparently , some unusual types of HIV have figured out how to use proteins other than CCR5 to invade cells .

显然，一些特殊的HIV想通了如何利用CCR5之外的蛋白入侵细胞。

Heterozygosity for CCR5 - △ 32 may confer partial protection against disease progression in HIV-inferent individuals .

而（CCR5-△32）半合子对HIV感染的个体的疾病进展则具有部分性保护作用。

Results Compared to B6 WT group , B6 CCR5 KO group succumbed to acute GVHD at an accelerated rate .

结果与B6WT组比较，B6CCR5KO组小鼠以更快的速度死于急性移植物抗宿主疾病（GVHD）；

He used a " zinc finger nuclease " Protein ( zinc finger protein ), stripping to T-cell surface of the CCR5 gene .

他采用一种名为“锌指核酸酶”的蛋白质（即锌指蛋白），来剥离T细胞表层的CCR5基因。

Objective : To study the relation of RANTES and its receptor ( CCR5 ) expression in gastric cancer and in lymph nodes with cancer metastasis .

目的：探讨RANTES及其受体（CCR5）在胃癌和转移淋巴结组织中的表达及其与胃癌转移的关系。

The CCR5 ribozyme molecule stops the patient 's white blood cells producing CCR5 , a protein that HIV uses to get into host cells .

这种CCR5核酶分子能中止了病人的白血细胞产生CCR5，后者是艾滋病毒用于进入宿主细胞的一种蛋白质。

Furthermore , expression of both CCR2 and CCR5 genes was enhanced significantly in activated macrophages when compared with non-activated macrophages .

而且，与未激活的巨噬细胞比较，已经激活的巨噬细胞CCR2，CCR5基因的表达增强更为明显。

After transplantation , only approximately 5 % to 8 % of the patient 's bone marrow cells carried the CCR5 edit , according to the researchers .

研究人员说，移植后，只有大约5%到8%的患者骨髓细胞携带这种经过编辑的基因。

Doctors sought out a donor with this rare genetic mutation , called CCR5 , which stops the HIV virus from attaching to infected cells .

医生们找到了一名具有这种罕见基因突变的人。这种基因突变叫做CCR5，能够阻止HIV病毒附着在感染细胞上。

Gene expression of CCR2 and CCR5 and their chemokines in transplanted FPP xenografts was evaluated by real-time PCR .

在移植了FPP异种移植物以后的CCR2，CCR5及它们的趋化因子的基因表达可通过实时PCR来评估。

This patient 's own cells had the usual amount of the CCR5 receptor , and the strain of HIV in his blood was the type that used the receptor .

回到这个研究中，这个患者存在着正常的CCR5基因，同时他所感染的病毒是利用这个基因复制的HIV类。

Since the patient was HIV-positive , researchers sought out a stem cell donor whose cells lacked the CCR5 receptor that HIV commonly uses to get into immune cells .

因为这个病人是艾滋病病毒感染者，科研学者找到了一个缺乏CCR5基因的细胞捐献者。提到CCR，这是一个HIV通常使用的通道来进入免疫细胞的。

Results Research showed that the coreceptor of the no HIV infected man had CCR5 △ 32 homozygote mutation which was not found whether among healthy person or HIV infected people .

结果抗HIV感染者发生CCR5△32纯合子突变，健康人及HIV感染者CCR5基因未发生突变。

Objective To evaluate the role of gene CCR5 on donor cells in models where intensive preconditioning of the recipient occurs , thus provide the scientific evidence for clinical experience of allo-HSCT .

本研究评价供者CCR5在经过强化预处理的骨髓移植动物模型受者体内的作用，为今后的异基因造血干细胞移植的临床应用提供科学依据。

The CCR5 gene mutation has been associated with a 21 % increased risk of dying early , according to a paper published in Nature in June , though it 's unclear why .

《自然》杂志今年6月发表的一篇论文称，CCR5基因突变与早逝风险增加21%有关，不过原因尚不清楚。

People who carry defective copies of CCR5 are highly immune to HIV , because the virus uses a protein made by this gene to gain entry into an infected person 's cells .

携带有发生突变的CCR5基因拷贝的人对艾滋病毒具有很高的免疫力，因为艾滋病毒利用这种基因产生的蛋白质进入感染者的细胞。

The team demonstrated that without this receptor , Mycobacterium tuberculosis was able to thrive inside host cells , as the immune cells did not receive the signal from CCR5 to attack them .

这个研究组证明了在没有这种受体的情况下，结核分枝杆菌可以在宿主细胞内大量生长，因为免疫细胞没有收到来自CCR5的进攻信号。

Fortunately , we know that certain people are indeed resistant to particular diseases . Take HIV , for example . Some people have a genetic mutation that disables their copy of the CCR5 protein .

幸运的是，我们知道某类人确实能够抵御特殊疾病。就拿HIV来说，一些人发生基因突变，使他们丧失了复制CCR5蛋白的能力。

Objective To investigate expression and significance of CC-chemokine receptor 5 ( CCR5 ) in HCV mono-infection , HIV mono-infection and HCV / HIV co-infection .

目的探讨T淋巴细胞表面C-C趋化因子受体5（CCR5）在丙型肝炎病毒（HCV）感染、人类免疫缺陷病毒（HIV）感染和HCV/HIV合并感染过程中的表达及意义。

Paul Lehner of the UK-based Cambridge Institute for Medical Research and colleagues identified a receptor on the host cells known as CCR5 that triggers the immune cells'response to tuberculosis ( TB ) .

英国剑桥医学研究所的PaulLehner和他的同事发现了人体宿主细胞上的一个称作CCR5的受体可以触发免疫细胞进攻结核菌。

HIV uses that protein as a doorway into human cells . So , if a person lacks CCR5 , HIV can 't enter their cells , and they 're extremely unlikely to become infected with the disease .

CCR5蛋白是HIV进入人体细胞的门户。因此，一个缺失CCR5的人，HIV便无法进入他的细胞内，从而使得他们避免遭受感染。