The IL-33/ST2 Axis Is Not Required for the Profibrotic Effect of IL-33 in the Lungs.
作者信息
Atamas Sergei P, Lockatell Virginia, Todd Nevins W, Luzina Irina G
机构信息
University of Maryland School of Medicine Baltimore, Maryland.
Baltimore Veterans Affairs Medical Center Baltimore, Maryland.
出版信息
Am J Respir Cell Mol Biol. 2024 Oct;71(4):499-501. doi: 10.1165/rcmb.2023-0434LE.
Abstract
摘要
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本文引用的文献
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The IL-33:ST2 axis is unlikely to play a central fibrogenic role in idiopathic pulmonary fibrosis.IL-33:ST2 轴在特发性肺纤维化中可能不起核心纤维化作用。
Respir Res. 2023 Mar 23;24(1):89. doi: 10.1186/s12931-023-02334-4.
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Full-length IL-33 augments pulmonary fibrosis in an ST2- and Th2-independent, non-transcriptomic fashion.全长 IL-33 以非转录组依赖性的方式增强 ST2 和 Th2 非依赖性的肺纤维化。
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The Idiopathic Pulmonary Fibrosis Cell Atlas.特发性肺纤维化细胞图谱
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The IL-33 Receptor ST2 Regulates Pulmonary Inflammation and Fibrosis to Bleomycin.白细胞介素-33受体ST2调节博来霉素所致的肺部炎症和纤维化。
Front Immunol. 2018 Jun 25;9:1476. doi: 10.3389/fimmu.2018.01476. eCollection 2018.
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Transcriptomic evidence of immune activation in macroscopically normal-appearing and scarred lung tissues in idiopathic pulmonary fibrosis.特发性肺纤维化中大体正常和瘢痕肺组织中免疫激活的转录组证据。
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IL-33 promotes ST2-dependent lung fibrosis by the induction of alternatively activated macrophages and innate lymphoid cells in mice.白细胞介素-33通过诱导小鼠体内替代性活化巨噬细胞和固有淋巴细胞，促进依赖于ST2的肺纤维化。
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Interleukin-33 potentiates bleomycin-induced lung injury.白细胞介素-33 增强博来霉素诱导的肺损伤。
Am J Respir Cell Mol Biol. 2013 Dec;49(6):999-1008. doi: 10.1165/rcmb.2013-0093OC.
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J Immunol. 2012 Jul 1;189(1):403-10. doi: 10.4049/jimmunol.1200259. Epub 2012 May 25.
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Diversity of airway epithelial cell targets for in vivo recombinant adenovirus-mediated gene transfer.体内重组腺病毒介导的基因转移的气道上皮细胞靶标的多样性。
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