CCR6 is not necessary for functional effects of human CCL18 in a mouse model.
CCR6 is not necessary for functional effects of human CCL18 in a mouse model.
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DOI：
10.1186/1755-1536-5-2
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发表时间：
2012-01-18
期刊：
影响因子：
--
通讯作者：
Atamas SP
中科院分区：
文献类型：
--
作者：
Luzina IG;Atamas SP
CCL18是一种未知受体的趋化因子，与几种与T淋巴细胞浸润相关的纤维化肺部疾病有关。据推测，CCL18可能通过CCR6起作用。人CCL18基因导入野生型小鼠肺内可诱导T淋巴细胞的肺内浸润，其中表达CCR6的T淋巴细胞不到5%。在CCR6基因缺陷小鼠的肺中，CCL18驱动的T淋巴细胞的浸润减弱，但并未完全消除。结论：CCR6在CCL18诱导的小鼠体内变化中不是必需的，CCR6不是该模型中CCL18的主要功能受体。
CCL18, a chemokine with no known receptor, has been implicated in several fibrotic pulmonary diseases associated with T-lymphocyte infiltration. It has been hypothesized that CCL18 may act through CCR6. Gene delivery of human CCL18 to the lungs of wild-type mice induced pulmonary infiltration of T-lymphocytes, less than 5% of which expressed CCR6. In the lungs of CCR6-deficient mice, CCL18-driven infiltration of T-lymphocytes was attenuated but not fully abrogated. It was concluded that CCR6 is not necessary for CCL18-induced changes in mice in vivo and that CCR6 is not the main functional receptor for CCL18 in this model.