The HIV co-receptor CCR5, regulates the cellular architecture of osteoclast

C-C chemokine receptor 5 (CCR5) is a co-receptor of HIV. Its ligand, CCL5 significantly augmented the number of wild-type osteoclasts but not Ccr5-deficient cells, indicating that CCL5 enhanced RANKL-induced osteoclastogenesis through CCR5. To investigate the changes in the transcriptional signatures induced by CCL5 in osteoclastogenesis, cultured osteoclasts at pOC stages were incubated with or without rmCCL5 for 2 days, and then subjected for RNA sequencing. mRNA profiles of primary bone marrow macrophages obtained from 7 weeks old C57BL6 mice were treated with recombinant CCL5, in triplicate, using Illumina Miseq.

C-C趋化因子受体5（C-C chemokine receptor 5, CCR5）是人类免疫缺陷病毒（HIV）的共受体。其配体C-C趋化因子配体5（CCL5）可显著上调野生型破骨细胞的数量，但对Ccr5基因缺陷型细胞无此作用，这表明CCL5通过CCR5增强核因子κB受体活化因子配体（RANKL）诱导的破骨细胞生成。为探究CCL5在破骨细胞生成过程中诱导的转录特征变化，我们将处于pOC阶段的培养破骨细胞分别用或不用重组CCL5（rmCCL5）孵育2天，随后进行RNA测序。本数据集的样本取自7周龄C57BL/6小鼠的原代骨髓巨噬细胞，经重组CCL5处理并设置三次生物学重复，采用Illumina Miseq平台完成测序。