在过敏性鼻炎中,Tet2通过mRNA5-甲基细胞素调节M2巨细胞极化
Wenjun Fan1, Peiqiang Liu1, Lu Tan1
1Department of Otolaryngology-Head and Neck Surgery, Renmin Hospital of Wuhan University, Wuhan, China.
International immunopharmacology
|November 1, 2024
概括
十-十一转位2 (Tet2) 酶缺乏会通过促进M2巨细胞两极化而加剧过敏性鼻炎. Tet2通过mRNA脱甲基化调节M2相关基因,为过敏炎症提供潜在的治疗点.
科学领域:
- 免疫学 免疫学 免疫学
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
- 过敏性疾病 过敏性疾病
背景情况:
- 过敏性鼻炎 (AR) 涉及免疫失衡和巨细胞异常活动.
- 替代激活的巨细胞 (M2) 与过敏病原发生有关.
- 十个十一个转位 (Tet) 酶调节RNA甲基化;Tet2在巨细胞两极化中的作用尚不清楚.
研究的目的:
- 研究Tet2在过敏炎症期间巨细胞两极化中的作用.
- 探索Tet2在AR中调节M2巨细胞极化中的机制.
主要方法:
- 分析了AR患者的鼻腔组织,以检测巨细胞两极分化和氨酸细胞数量.
- 利用Raw264.7细胞研究Tet2,mRNA甲基化和巨细胞极化.
- 使用野生类型和Tet2淘汰赛小鼠建立了卵白蛋白 (OVA) 诱导的AR小鼠模型.
- 在骨髓衍生的巨细胞 (BMDMs) 上执行RNA测序和MeRIP-qPCR,以评估M2相关基因的mRNA甲基化.
主要成果:
- 在AR鼻腔组织中,M2巨细胞和埃索诺菲尔细胞普遍存在.
- 在体外,Tet2表达和mRNA甲基化与M2巨细胞两极化相关.
- Tet2 缺乏症加重了AR的严重程度,并改变了巨细胞的两极分化.
- Tet2 缺乏减少了 Klf4 和 Rock1 的 mRNA m5C 脱甲基化,促进了 M2 极化.
结论:
- Tet2通过通过mRNA m5C脱甲基化抑制M2极化,在AR中起着保护作用.
- 通过Tet2在转录后水平上准巨细胞两极分化为AR提供了一个新的治疗策略.
相关概念视频
02:23Master Transcription Regulators
6.9K
Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...
6.9K
01:24T Cell Types and Functions
954
When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
954
01:26Asthma-II: Pathophysiology and Classification
2.6K
Asthma is a prevalent chronic respiratory condition marked by inflammation and hyperresponsiveness of the airways. Its pathophysiology involves complex interactions among inflammatory pathways, immune responses, and neural mechanisms.
Additionally, environmental and genetic factors play crucial roles in determining an individual's susceptibility to asthma and the severity of their condition.
Critical processes in asthma pathophysiology include:
Additionally, environmental and genetic factors play crucial roles in determining an individual's susceptibility to asthma and the severity of their condition.
Critical processes in asthma pathophysiology include:
2.6K