Expression and regulation of chemokine receptors in human natural killer cells
Expression and regulation of chemokine receptors in human natural killer cells
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DOI：
10.1182/blood.v97.2.367
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发表时间：
2001-01-15
期刊：
影响因子：
20.3
通讯作者：
Maghazachi, AA
中科院分区：
文献类型：
--
作者：
Inngjerdingen, M;Damaj, B;Maghazachi, AA
利用流式细胞术和RNase保护实验，本研究检测了趋化因子受体在非活化的自然杀伤（NK）细胞中的表达，并将其与白细胞介素(IL)-2活化的NK细胞的表达进行了比较，这些NK细胞亚群中没有表达CXCR2、CXCR5或CCR5，这些细胞之间的主要差异包括CXCR1、CCR1、CCR2、CCR4、CCR8的表达增加，而CXCR1、CCR1、CCR2、CCR4、CCR8的表达增加。与NA或非活化NK细胞相比，AD中的CX(3)CR1。对CXC和CC趋化因子的趋化反应与受体表达相关，除了所有3个种群都对gro - α有反应，尽管它们缺乏CXCR2的表达。用抗cxcr2预处理这些细胞并没有抑制对gro - α的趋化反应，此外，非激活细胞和NA细胞对fractalkine有反应，尽管它们缺乏CX(3)CR1的表达。抗cx (3)CR1不抑制该活性。病毒巨噬细胞炎症蛋白(vip)-I、I-309和TARC以不同的亲和力与I-125-309结合AD细胞竞争。转化生长因子(TGF)- β 1上调NK细胞表面CXCR3和CXCR4的表达，但未检测其他细胞因子或趋化因子，包括干扰素(IFN)- γ、MIP-3 β、巨噬细胞来源趋化因子（MDC）、胸腺和激活调节趋化因子（TARC）或I-309。这与tgf - β 1处理NK细胞对基质细胞衍生因子(SDF)-1 α和干扰素诱导蛋白（IP-10）、淋巴趋化蛋白信使RNA、RANTES、MIP-1 α和MIP-1 β的趋化性增加有关，但不包括IP-10、单核细胞趋化蛋白(MCP)-1、IL-8或I-309在所有3个NK细胞亚群中表达。我们的结果可能对NK细胞在肿瘤生长或病毒复制部位的传播有影响。(C) 2001年由美国血液学会出版。
Using flow cytometric and RNase protection assays, this study examined the expression of chemokine receptors in nonactivated natural killer (NK) cells and compared this expression with NK cells activated with interleukin (IL)-2, which either adhered to plastic flasks (AD) or did not adhere (NA), None of the NK cell subsets expressed CXCR2, CXCR5, or CCR5, The major differences between these cells include increased expression of CXCR1, CCR1, CCR2, CCR4, CCR8, and CX(3)CR1 in AD when compared to NA or nonactivated NK cells. The chemotactic response to the CXC and CC chemokines correlated with the receptor expression except that all 3 populations responded to GRO-alpha, despite their lack of CXCR2 expression. Pretreatment of these cells with anti-CXCR2 did not inhibit the chemotactic response to GRO-alpha, In addition, nonactivated and NA cells responded to fractalkine, although they lack the expression of CX(3)CR1. This activity was not inhibited by anti-CX(3)CR1. Viral macrophage inflammatory protein (vMIP)-I, I-309, and TARC competed with the binding of I-125-309 to AD cells with varying affinities. Transforming growth factor(TGF)-beta1 but not any other cytokine or chemokine examined including interferon (IFN)-gamma, MIP-3 beta, macrophage-derived chemokine (MDC), thymus and activation-regulated chemokine (TARC) or I-309, up-regulated the expression of CXCR3 and CXCR4 on NK cell surface. This is correlated with increased chemotaxis of NK cells treated with TGF-beta1 toward stromal cell-derived factor (SDF)-1 alpha and interferon-inducible protein-in (IP-10), Messenger RNA for lymphotactin, RANTES, MIP-1 alpha, and MIP-1 beta, but not IP-10, monocyte chemotactic protein (MCP)-1, IL-8, or I-309 was expressed in all 3 NK cell subsets. Our results may have implications for the dissemination of NK cells at the sites of tumor growth or viral replication. (C) 2001 by The American Society of Hematology.