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T regulatory cells and attenuated bleomycin-induced fibrosis in lungs of CCR7-/- mice

机译:CCR7-/-小鼠肺部T调节细胞和博莱霉素减毒诱导的纤维化

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摘要

BackgroundC-C chemokine receptor (CCR)7 is a regulator of dendritic cell and T cell migration, and its role in tissue wound healing has been investigated in various disease models. We have previously demonstrated that CCR7 and its ligand, chemokine (C-C motif) ligand (CCL)21, modulates wound repair in pulmonary fibrosis (PF) but the mechanism of this is unknown. The objective of this study was to investigate whether the absence of CCR7 protects against bleomycin (BLM)-induced PF. CCR7-/- mice failed to mount a fibrotic pulmonary response as assessed by histologic collagen staining and quantification by hydroxyproline. We hypothesized that the prominent characteristics of CCR7-/- mice, including elevated levels of cytokine and chemokine mediators and the presence of bronchus-associated lymphoid tissue (BALT) might be relevant to the protective phenotype.
机译:背景C-C趋化因子受体(CCR)7是树突状细胞和T细胞迁移的调节剂,已在多种疾病模型中研究了其在组织伤口愈合中的作用。我们以前已经证明,CCR7及其配体趋化因子(CC配体)配体(CCL)21可以调节肺纤维化(PF)中的伤口修复,但其机制尚不清楚。这项研究的目的是调查是否缺少CCR7可以预防博来霉素(BLM)诱导的PF。通过组织学胶原染色和羟脯氨酸定量评估,CCR7 -/-小鼠未能发生纤维化性肺反应。我们假设CCR7 -//-小鼠的显着特征,包括细胞因子和趋化因子介质水平升高以及支气管相关淋巴样组织(BALT)的存在可能与保护性表型有关。

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