ZFP36 家族的表达受到哮喘 Th2 细胞的抑制,导致炎症细胞因子和细胞表面分子的合成增强。

IF 3.7 4区 医学 Q2 CELL BIOLOGY
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引用次数: 0

摘要

哮喘是一种慢性气道炎症性疾病,其中炎性细胞因子起着关键作用。锌指结合蛋白 36(ZFP36)家族包括 ZFP36、ZFP36L1 和 ZFP36L2,是据报道可导致炎症的 RNA 结合蛋白(RBPs)之一。本研究旨在阐明 ZFP36 家族在哮喘中的作用,特别是强调 ZFP36 家族与 Th2 细胞之间的关系,Th2 细胞是哮喘中 2 型炎症的主要参与者。实时 PCR 分析显示,ZFP36 家族 mRNA 在人类白细胞中优先表达。利用GEO数据库(https://www.ncbi.nlm.nih.gov/gds)的公开数据集进行的基因表达分析表明,与健康对照组相比,哮喘患者体内ZFP36家族mRNA的表达明显受到抑制。通过多种细胞因子检测,用 ZFP36 家族 siRNAs 转染 Th2 细胞可提高炎症细胞因子 IL-8、IFN-γ、CCL3/MIP-1α、CCL4/MIP-1β 和 TNF-α,以及细胞表面分子 CCR4 (CD194) 和 PSGL-1 (CD162) 的表达。用 IL-2、4 和 15 治疗可明显抑制 Th2 细胞对 ZFP36 家族 mRNA 的表达,而皮质类固醇可明显增强 Th2 细胞对 ZFP36 家族 mRNA 的表达。总之,哮喘患者 Th2 细胞表达的 ZFP36 家族受到抑制,导致细胞因子和细胞表面分子的表达增强。哮喘患者的 ZFP36 表达受抑制可能与气道炎症的增强有关,ZFP36 家族可能是包括哮喘在内的炎症性疾病的治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
ZFP36 family expression is suppressed by Th2 cells in asthma, leading to enhanced synthesis of inflammatory cytokines and cell surface molecules

Asthma is a chronic inflammatory airway disease, in which inflammatory cytokines play a pivotal role. The zinc finger binding protein 36 (ZFP36) family includes ZFP36, ZFP36L1, and ZFP36L2 and is among the RNA-binding proteins (RBPs) reported to cause inflammation. The present study aimed to clarify the roles of the ZFP36 family in asthma, particularly highlighting the relationship between the ZFP36 family and Th2 cells, which are key players in type 2 inflammation in asthma. Real-time PCR analysis revealed the preferential expression of ZFP36 family mRNAs in human white blood cells. Gene expression analysis using public datasets from the GEO database (https://www.ncbi.nlm.nih.gov/gds) showed significantly suppressed expression of ZFP36 family mRNAs in patients with asthma compared to that in healthy controls. Using multiple cytokine assays, Th2 cell transfection with ZFP36 family siRNAs enhanced the expression of inflammatory cytokines IL-8, IFN-γ, CCL3/MIP-1α, CCL4/MIP-1β, and TNF-α and cell surface molecules CCR4 (CD194) and PSGL-1 (CD162). Treatment with IL-2, 4, and 15 significantly suppressed, and corticosteroid significantly enhanced the expressions of ZFP36 family mRNAs by Th2 cells. In conclusion, the ZFP36 family expressed by Th2 cells was suppressed in patients with asthma, leading to the enhanced expression of cytokines and cell surface molecules. Suppressed ZFP36 expression in asthma may be involved in the enhancement of airway inflammation, and the ZFP36 family may be a therapeutic target for inflammatory diseases, including asthma.

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来源期刊
Cellular immunology
Cellular immunology 生物-免疫学
CiteScore
8.20
自引率
2.30%
发文量
102
审稿时长
30 days
期刊介绍: Cellular Immunology publishes original investigations concerned with the immunological activities of cells in experimental or clinical situations. The scope of the journal encompasses the broad area of in vitro and in vivo studies of cellular immune responses. Purely clinical descriptive studies are not considered. Research Areas include: • Antigen receptor sites • Autoimmunity • Delayed-type hypersensitivity or cellular immunity • Immunologic deficiency states and their reconstitution • Immunologic surveillance and tumor immunity • Immunomodulation • Immunotherapy • Lymphokines and cytokines • Nonantibody immunity • Parasite immunology • Resistance to intracellular microbial and viral infection • Thymus and lymphocyte immunobiology • Transplantation immunology • Tumor immunity.
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