肌成纤维细胞的形成及活化是肺纤维化的主要病理特征，先前的研究提示趋化因子CXCL16及其受体CXCR6在诱导肌成纤维细胞形成及促进纤维化中起重要作用。我们的前期研究也发现结缔组织病（CTD）合并肺纤维化的患者较单纯CTD患者血清中CXCL16显著升高，提示CXCL16可能在肺纤维化发病中发挥一定作用，但机制尚不清楚。本研究拟从细胞和分子水平，初次系统探讨CXCL16/CXCR6轴在肺泡上皮细胞和肺成纤维细胞向肌成纤维细胞转化中的作用和机制；同时利用博来霉素诱导肺纤维化模型小鼠，体内证实CXCL16/CXCR6轴促进纤维化的作用，并充分探讨其中的分子机制。据此，揭示CXCL16/CXCR6轴在肺纤维化致病中的作用和机制，为深入理解结缔组织病相关肺纤维化发病机制提供了新的视角，为其治疗提供新的靶点。

The formation and activation of myofibroblasts is the main pathological feature of pulmonary fibrosis. Previous studies suggest that chemokine CXCL16 and its receptor CXCR6 play an important role in inducing the formation of myofibroblasts and promoting fibrosis. Our previous study also found that serum CXCL16 level in patients with connective tissue disease (CTD) associated pulmonary fibrosis was significantly higher than that in patients with simple CTD, suggesting that CXCL16 may play a role in the pathogenesis of pulmonary fibrosis, but the mechanism is unclear. This study intend to investigate the role and mechanism of CXCL16/CXCR6 axis in the transformation of alveolar epithelial cells and lung fibroblasts into myofibroblasts from the cell and molecular level. At the same time, bleomycin-induced pulmonary fibrosis model mice were used to verify the effect and mechanism of CXCL16/CXCR6 axis in pulmonary fibrosis. The systematic study of the CXCL16/CXCR6 axis may provide a new perspective for profound understanding of the pathogenesis of connective tissue disease associated pulmonary fibrosis. This study provides a new target for the treatment of connective tissue disease associated pulmonary fibrosis.