转录组研究揭示了系统性红斑狼疮分子和细胞的复杂性:综述

IF 4.5 3区 医学 Q2 IMMUNOLOGY
Frank Qingyun Wang, Xiao Dang, Wanling Yang
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引用次数: 0

摘要

系统性红斑狼疮(SLE)是一种复杂的自身免疫性疾病,临床表现多种多样。这种方法为了解系统性红斑狼疮发病机制中的基因表达模式和分子调控机制提供了宝贵的信息。值得注意的是,干扰素刺激基因(ISG)特征在免疫细胞、皮肤和肾脏中明显上调。虽然有人提出了与血清学参数和临床症状的相关性,但与整体疾病活动的关联仍存在争议。该领域的主要发现包括与疾病活动呈正相关的浆细胞特征上调;与狼疮肾炎相关的中性粒细胞特征;以及反映淋巴细胞减少的淋巴细胞特征下降。组织层面的研究强调了浸润免疫细胞在器官损伤中的关键作用。未来的研究应利用先进技术并整合多组学数据,以加深我们对系统性红斑狼疮分子基础的了解,从而促进靶向疗法的开发。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Transcriptomic studies unravel the molecular and cellular complexity of systemic lupus erythematosus: A review

Transcriptomic analysis plays a vital role in investigating Systemic Lupus Erythematosus (SLE), a complex autoimmune disease characterized by diverse clinical manifestations. This approach has yielded valuable insights into gene expression patterns and molecular regulatory mechanisms involved in SLE pathogenesis. Notably, interferon-stimulated gene (ISG) signatures are significantly upregulated in immune cells, skin, and kidney. Although a correlation with serological parameters and clinical symptoms has been proposed, the association with global disease activities remains controversial. Key findings in the field include an upregulated plasmablast signature, which positively correlates with disease activity; a neutrophil signature associated with lupus nephritis; and a decreased lymphocyte signature, reflecting lymphopenia. Tissue-level studies highlight the critical role of infiltrating immune cells in organ damage. Future research should leverage advanced technologies and integrate multi-omics data to deepen our understanding of SLE's molecular underpinnings, facilitating the development of targeted therapies.

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来源期刊
Clinical immunology
Clinical immunology 医学-免疫学
CiteScore
12.30
自引率
1.20%
发文量
212
审稿时长
34 days
期刊介绍: Clinical Immunology publishes original research delving into the molecular and cellular foundations of immunological diseases. Additionally, the journal includes reviews covering timely subjects in basic immunology, along with case reports and letters to the editor.
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