T-cells in the cerebrospinal fluid express a similar repertoire of inflammatory chemokine receptors in the absence or presence of CNS inflammation:: implications for CNS trafficking
T-cells in the cerebrospinal fluid express a similar repertoire of inflammatory chemokine receptors in the absence or presence of CNS inflammation:: implications for CNS trafficking
复制标题
DOI：
10.1046/j.1365-2249.2002.01947.x
复制
发表时间：
2002-09-01
影响因子：
4.6
通讯作者：
Ransohoff, RM
中科院分区：
文献类型：
--
作者：
Kivisäkk, P;Trebst, C;Ransohoff, RM
据信趋化因子及其受体参与T细胞向中枢神经系统（CNS）的运输。本研究的目的是确定与运输到炎症部位相关的六种趋化因子受体在脑脊液（CSF）T细胞上的表达。流式细胞术检测趋化因子受体表达。我们观察到CSF中的CD 3 + T细胞表达一系列有限的炎症趋化因子受体，特别是CXCR 3、CCR 5和CCR 6，但很少表达CCR 1 -3。这是独立的存在中枢神经系统炎症，因为类似的结果，在多发性硬化症（MS）患者和非炎症性神经系统疾病的个人。CCR 5 + T细胞在CSF中的富集可以在很大程度上解释为该隔室中较高频率的CD 4 +/CD 45 RO + T细胞。相反，与血液相比，表达CXCR 3的CD 4 +/CD 45 RO + T细胞在CSF中显著富集。在血液和CSF中观察到相似的CCR 6 +/CD 3 + T细胞水平，而CSF中的CCR 2 +/CD 3 + T细胞水平低于血液。CSF实际上缺乏CCR 5 +/CXCR 3-T细胞，表明单独的CCR 5表达不足以将CD 3 + T细胞运输至CSF。我们假设CXCR 3是参与MS中T细胞鞘内积聚的主要炎性趋化因子受体。通过与其配体的相互作用，CXCR 3被提议介导T细胞在发炎CNS中的保留。
It is believed that chemokines and their receptors are involved in trafficking of T-cells to the central nervous system (CNS). The aim of the current study was to define the expression on cerebrospinal fluid (CSF) T-cells of six chemokine receptors associated with trafficking to sites of inflammation. Flow cytometry was used to detect chemokine receptor expression. We observed that CD3+T-cells in the CSF express a restricted array of inflammatory chemokine receptors, specifically CXCR3, CCR5 and CCR6, but little CCR1-3. This repertoire was independent of the presence of CNS inflammation, since comparable findings were obtained in patients with multiple sclerosis (MS) and individuals with non-inflammatory neurological diseases. The enrichment of CCR5+T-cells in the CSF could largely be explained by higher frequency of CD4+/CD45RO+T-cells in this compartment. In contrast, CD4+/CD45RO+T-cells expressing CXCR3 were significantly enriched in CSF as compared with blood. Similar levels of CCR6+/CD3+T-cells were observed in blood and CSF, while levels of CCR2+/CD3+T-cells were lower in CSF than in blood. The CSF was virtually devoid of CCR5+/CXCR3- T-cells, suggesting that the expression of CCR5 alone is not sufficient for the trafficking of CD3+T-cells to the CSF. We hypothesize that CXCR3 is the principal inflammatory chemokine receptor involved in intrathecal accumulation of T-cells in MS. Through interactions with its ligands, CXCR3 is proposed to mediate retention of T-cells in the inflamed CNS.