A&R:白细胞介素4诱导的上皮细胞衰老对IgG4相关性唾液腺炎的新治疗靶点

2022-06-23 彼岸河边草 MedSci原创

IL-4通过活性氧(ROS)/p38 MAPK-p16 INK4A通路诱导的细胞衰老促进IgG4相关唾液腺炎(IgG4-RS)的纤维化。

目的IgG4相关疾病(IgG4-RD)是一种全身性纤维炎症性疾病,其特征是唾液腺、胰腺、泪腺和肾脏等多个器官中IgG4+浆细胞浸润增加和席纹状纤维化。IgG4相关唾液腺炎(IgG4-RS)是一种以腺体纤维化和唾液分泌不足为特征的慢性纤维炎性疾病。本研究旨在探讨细胞衰老在IgG4-RS相关纤维化发病机制中的作用。

方法:通过蛋白质组学、实时聚合酶链反应、蛋白质印迹和免疫组织化学测定IgG4-RS患者(n=18)和对照(n=14)的颌下腺(SMG)衰老标志物和促炎细胞因子的表达。在白细胞介素 4 (IL-4)处理后,进行高通量RNA测序以鉴定SMG-C6细胞(具有腺泡细胞特征的大鼠颌下皮细胞系)中的差异表达基因。通过将 IL-4腺内注射到小鼠颌下腺中建立腺体纤维化模型(每组n=8)。

结果唾液腺泡和导管上皮细胞在IgG4-RS患者中发生衰老,衰老相关的β-半乳糖苷酶活性升高、脂褐质积累、衰老标志物(p53p16INK4A)的表达增强以及衰老相关的分泌表型因子上调。此外,来自IgG4-RS患者的SMGIL-4水平显著增加(P<0.01),这与p16INK4A表达和纤维化评分呈正相关。IL-4通过活性氧(ROS)/p38 MAPK途径增加 p16INK4A 的表达,加剧了唾液上皮细胞衰老。IL-4诱导的衰老SMG-C6细胞收集的上清液增强了成纤维细胞的活化和基质蛋白的产生(P<0.05)。此外,给小鼠注射IL-4可促进颌下腺的纤维化和衰老表型。

结论IL-4通过ROS/p38 MAPK-p16INK4A通路诱导的细胞衰老促进IgG4-RS的纤维化。该研究的数据表明,细胞衰老可以作为治疗IgG4-RS的新治疗靶点。

出处:Min, S.-N., Zhu, M.-Q., Mao, X.-D., Li, W., Wei, T., Mei, M., Zhang, Y., Wu, L.-L., Yu, G.-Y. and Cong, X. (2022), Contribution of Interleukin-4–Induced Epithelial Cell Senescence to Glandular Fibrosis in IgG4-Related Sialadenitis. Arthritis Rheumatol, 74: 1070-1082. https://doi.org/10.1002/art.42052

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    2022-06-24 1de78fb9m22(暂无匿称)

    病理学论据,需补充

    0

  5. 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