T cell chemokine receptor expression in human Th1- and Th2-associated diseases.

T cell chemokine receptor expression in human Th1- and Th2-associated diseases.
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人类 Th1 和 Th2 相关疾病中 T 细胞趋化因子受体的表达。

DOI:
10.1007/978-94-015-9702-9_3
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发表时间:
2000
影响因子:
3.2
通讯作者:
K. HayGlass
K. HayGlass
中科院分区:
医学4区
文献类型:
--
作者:
J. D. Campbell;K. HayGlass

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趋化因子及其受体之间的相互作用是控制白细胞向炎症部位迁移的重要步骤。趋化因子还介导多种不依赖于趋化作用的效应,包括诱导和增强Th1和Th2相关的细胞因子反应。最近的研究表明,在体外多克隆刺激的极化条件下,人类Th1和Th2克隆表现出不同的趋化因子受体表达模式:Th1克隆优先表达CCR5和CXCR3,而许多Th2克隆表达CCR4、CCR8,少量表达CCR3。趋化因子受体表达的这些不同模式表明,在炎症和正常免疫稳态期间,有选择地诱导Th1和Th2型细胞迁移和激活的机制。研究已经开始检测T细胞趋化因子受体在体内的表达,以确定这些体外观察与人类Th1和Th2相关疾病的相关性。在这篇综述中,我们对T细胞趋化因子受体在人类自身免疫性疾病(多发性硬化症和类风湿性关节炎)和特应性疾病(过敏性鼻炎和哮喘)中表达的最新报道进行了综述,这些疾病被认为分别是由不适当的Th1和Th2主导的反应引起的。
The interaction between chemokines and their receptors is an important step in the control of leukocyte migration into sites of inflammation. Chemokines also mediate a variety of effects independent of chemotaxis, including induction and enhancement of Th1- and Th2-associated cytokine responses. Recent studies have shown that human Th1 and Th2 clones, activated under polarizing conditions with polyclonal stimuli in vitro, display distinct patterns of chemokine receptor expression: Th1 clones preferentially express CCR5 and CXCR3, while many Th2 clones express CCR4, CCR8 and, to a lesser extent, CCR3. These differential patterns of chemokine receptor expression suggest a mechanism for selective induction of migration and activation of Th1- and Th2-type cells during inflammation and, perhaps, normal immune homoeostasis. Studies have begun to examine T cell chemokine receptor expression in vivo to determine the relevance of these in vitro observations to human Th1- and Th2-associated diseases. In this review, we critically examine recent reports of T cell chemokine receptor expression in human autoimmune disorders (multiple sclerosis and rheumatoid arthritis) and atopic disorders (allergic rhinitis and asthma) which are believed to arise from inappropriate Th1- and Th2-dominated responses, respectively.
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发表时间: 1999-12-01
影响因子: 24.7
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发表时间: 1999-06-08
影响因子: 11.1
作者:
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通讯作者: Hancock, WW