Involvement of beta-chemokines in the development of inflammatory demyelination.
Involvement of beta-chemokines in the development of inflammatory demyelination.
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DOI：
10.1186/1742-2094-2-7
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发表时间：
2005-02-24
影响因子：
9.3
通讯作者：
Kalman B
中科院分区：
文献类型：
--
作者：
Banisor I;Leist TP;Kalman B
β-趋化因子（或CC趋化因子配体- CCL）在多发性硬化症患者和实验性过敏性脑脊髓炎啮齿动物中枢神经系统炎性病变发展中的重要性得到描述性研究和实验模型的有力支持。我们最近对家族进行的基因扫描确定了CCL 2、CCL 3和CCL 11-CCL 8-CCL 13基因的单倍型，这些基因与多发性硬化症有关。作为对遗传关联的补充，我们还检测到CCL 2、CCL 7和CCL 8与多发性硬化症大脑中慢性炎症相关的独特区域表达调节。这些观察结果与以前的研究一致，并增加了新的数据来支持CCL 2，CCL 7，CCL 8和CCL 3参与炎症性脱髓鞘的发展。沿着我们自己的数据，在这里，我们回顾了文献牵连CCL及其受体（CCR）在多发性硬化症和实验性过敏性脑脊髓炎。该调查反映了该领域正在迅速扩张，并强调了一些可能适合药物干预的途径。
The importance of β-chemokines (or CC chemokine ligands – CCL) in the development of inflammatory lesions in the central nervous system of patients with multiple sclerosis and rodents with experimental allergic encephalomyelitis is strongly supported by descriptive studies and experimental models. Our recent genetic scans in families identified haplotypes in the genes of CCL2, CCL3 and CCL11-CCL8-CCL13 which showed association with multiple sclerosis. Complementing the genetic associations, we also detected a distinct regional expression regulation for CCL2, CCL7 and CCL8 in correlation with chronic inflammation in multiple sclerosis brains. These observations are in consensus with previous studies, and add new data to support the involvement of CCL2, CCL7, CCL8 and CCL3 in the development of inflammatory demyelination. Along with our own data, here we review the literature implicating CCLs and their receptors (CCRs) in multiple sclerosis and experimental allergic encephalomyelitis. The survey reflects that the field is in a rapid expansion, and highlights some of the pathways which might be suitable to pharmaceutical interventions.
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