免疫相关疾病的IL-33遗传学和表观遗传学。

Eleonora Di Salvo, Marco Casciaro, Sebastiano Gangemi
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引用次数: 3

摘要

白细胞介素-33 (IL-33)是一种30KDa的蛋白,属于白细胞介素-1细胞因子家族。它是先天和适应性免疫反应的重要调节因子。这种白细胞介素还参与对抗蠕虫感染的炎症反应。白细胞介素33作用于2组先天淋巴样细胞、肥大细胞、巨噬细胞、树突状细胞和CD4 + Th2细胞,引起2型免疫应答。此外,该细胞因子可以激活Tregs的ST2,表明其具有下调炎症的能力。IL-33还通过调节转录具有细胞内功能。活跃的IL-33没有信号肽,所以它不会通过正常的分泌途径释放;当细胞受损时,白细胞介素就会释放出来,起到“警报”的作用。它对免疫激活的影响可以通过涉及级联途径和免疫基因的精细表观遗传相互作用进行微调。由于来自不同实验研究的数据不同,我们决定跨越文献尽可能地阐明IL-33是如何受到基因表达的影响和影响的。根据所考虑的组织,作者报告了其平衡是如何受到影响的。IL-33是免疫相关疾病的基础,在控制炎症中起关键作用。在不久的将来,对细胞因子开关的理解将是阻断或激活某些免疫途径的基础。事实上,我们不仅可以通过单克隆抗体来控制白介素的作用,还可以通过siRNA或miRNAs来沉默或表达关键基因。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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IL-33 genetics and epigenetics in immune-related diseases.

Interleukin-33 (IL-33) is a 30KDa protein, which belongs to the Interleukin-1 cytokine family. It is a crucial regulator of innate and adaptive immune responses. This interleukin is additionally involved in the inflammatory reaction versus helminthic infections. Interleukin 33 acts on group 2 innate lymphoid cells and mast cells macrophages, dendritic cells and CD4 + Th2 cells eliciting a type 2 immune response. Moreover, the cytokine can activate the ST2 of Tregs, demonstrating its ability to downregulate inflammation. IL-33 has also an intracellular function by regulating transcription. The active IL-33 doesn't have a signal peptide, so it's not released across a normal secretory pathway; the interleukin is released when the cells are damages and acts like an "alarmin". Its influence on immune activation could be slightly adjusted via fine epigenetic interactions involving cascade pathways and immune genes. Due to the diverse data emerged from different experimental research, we decided span literature to clarify, as much as possible, how IL-33 is influenced by and influence gene expression. The authors reported how its balance is influenced, according to the tissue considered. Fundamental for immune-related diseases, IL-33 has a key role in controlling inflammation. The understanding of the cytokine switch will be fundamental in a near future in order to block or activate some immune pathways. In fact, we could control interleukins effects not only by monoclonal antibodies but also by using siRNA or miRNAs for silencing or expressing key genes.

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来源期刊
Clinical and Molecular Allergy
Clinical and Molecular Allergy Medicine-Immunology and Allergy
CiteScore
8.20
自引率
0.00%
发文量
11
审稿时长
13 weeks
期刊介绍: Clinical and Molecular Allergy is an open access, peer-reviewed, online journal that publishes research on human allergic and immunodeficient disease (immune deficiency not related to HIV infection/AIDS). The scope of the journal encompasses all aspects of the clinical, genetic, molecular and inflammatory aspects of allergic-respiratory (Type 1 hypersensitivity) and non-AIDS immunodeficiency disorders. However, studies of allergic/hypersensitive aspects of HIV infection/AIDS or drug desensitization protocols in AIDS are acceptable. At the basic science level, this includes original work and reviews on the genetic and molecular mechanisms underlying the inflammatory response.
期刊最新文献
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