Suppr超能文献

基于前瞻性队列研究探讨与 Takayasu 动脉炎不同临床特征相关的分子特征。

Exploration of molecular signatures associated with different clinical features of Takayasu arteritis based on a prospective cohort study.

机构信息

Department of Rheumatology, Zhongshan Hospital, Fudan University, Shanghai, China.

Department of Rheumatology, Zhongshan Hospital, Fudan University, Shanghai, China; Center of Clinical Epidemiology and Evidence-based Medicine, Fudan University, Shanghai, China.

出版信息

Clin Immunol. 2023 Nov;256:109794. doi: 10.1016/j.clim.2023.109794. Epub 2023 Sep 27.

Abstract

Takayasu arteritis (TAK) is complicated disorder without reliable biomarkers. Here, we aimed to explore TAK-associated factor panels and their changes after biologic treatment. Five factor panels were identified: 1. systemic inflammation: C3, ESR, CRP, PLT, IL-6, C4, and IgG; 2. vascular inflammation: YKL40, IL-16, PTX3, and CCL2; 3. immune regulation panel: IL-10, IFN-γ, CCL5, and MMP1; 4. angiogenesis and fibrosis: FGF, PDGFAB, and VEGF; and 5. vascular remodeling: CD19+ B cell ratio, MMP3, and leptin. Panel 1 parameters were closely related to disease activity, while Panel 5 parameters, particularly CD19+ B cell ratio and leptin, were significantly higher in ischemic patients. After treatment, tocilizumab had a stronger inhibitory effect on Panel 1 parameters, PTX3, and YKL-40, while adalimumab led to an increase in IL-16, CCL2, and leptin levels. Altogether, these data expanded our knowledge regarding molecular background in TAK development and shed light on precise treatment in future studies.

摘要

Takayasu 动脉炎(TAK)是一种复杂的疾病,没有可靠的生物标志物。在这里,我们旨在探讨 TAK 相关的因子谱及其在生物治疗后的变化。确定了五个因子谱:1. 全身炎症:C3、ESR、CRP、PLT、IL-6、C4 和 IgG;2. 血管炎症:YKL40、IL-16、PTX3 和 CCL2;3. 免疫调节谱:IL-10、IFN-γ、CCL5 和 MMP1;4. 血管生成和纤维化:FGF、PDGFAB 和 VEGF;5. 血管重塑:CD19+B 细胞比、MMP3 和瘦素。第 1 组参数与疾病活动密切相关,而第 5 组参数,特别是 CD19+B 细胞比和瘦素,在缺血患者中明显升高。治疗后,托珠单抗对第 1 组参数、PTX3 和 YKL-40 有更强的抑制作用,而阿达木单抗导致 IL-16、CCL2 和瘦素水平升高。总的来说,这些数据扩展了我们对 TAK 发展分子背景的认识,并为未来的研究提供了精确治疗的启示。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验