Luzina Irina G, Atamas Sergei P
Department of Medicine, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
Fibrogenesis Tissue Repair. 2012 Jan 18;5(1):2. doi: 10.1186/1755-1536-5-2.
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.
CCL18是一种没有已知受体的趋化因子，它与几种伴有T淋巴细胞浸润的纤维化肺部疾病有关。据推测，CCL18可能通过CCR6发挥作用。将人CCL18基因导入野生型小鼠肺部可诱导T淋巴细胞的肺部浸润，其中表达CCR6的细胞不到5%。在CCR6缺陷小鼠的肺部，CCL18驱动的T淋巴细胞浸润减弱但并未完全消除。得出的结论是，CCR6对于CCL18在小鼠体内诱导的变化并非必需，且在该模型中CCR6不是CCL18的主要功能受体。
