Biological mechanisms and therapeutic prospects of interleukin-33 in pathogenesis and treatment of allergic disease.

IF 4.4 3区 医学 Q2 IMMUNOLOGY
Mohammad Chand Jamali, Asma'a H Mohamed, Azfar Jamal, Mohammad Azhar Kamal, Waleed Al Abdulmonem, Bashar Abdullah Saeed, Nasrin Mansuri, Fuzail Ahmad, Mustafa Mudhafar, Alaa Shafie, Haroonrashid M Hattiwale
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Abstract

Allergic diseases significantly impact the quality of life of people around the world. Cytokines play a crucial role in regulating the immune system. Due to their importance in pro-inflammatory mechanisms, cytokines are used to understand pathogenesis and serve as biomarkers in many diseases. One such cytokine is interleukin-33, a member of the IL-1 family, including IL- 1α, IL-1β, and IL-18. The IL-33 receptor is a heterodimer of IL-1 receptor-like 1 and IL-1 receptor accessory protein. IL-33 plays a critical role in regulating innate and adaptive immune responses. The primary targets of IL-33 in vivo are tissue-resident immune cells, including mast cells, group 2 innate lymphoid cells, regulatory T cells, T helper 2 cells, eosinophils, basophils, dendritic cells, Th1 cells, CD8 + T cells, NK cells, iNKT cells, B cells, neutrophils, and macrophages. However, IL-33 appears to act as an alarm signal that is promptly released by producing cells under cellular damage or stress conditions. IL-33 regulates signaling and various biological functions, including induction of pro-inflammatory cytokines, regulation of cell proliferation, and involvement in tissue remodeling. IL-33 is fundamental in immune-related diseases and plays a critical role in the control of inflammation. Recently, IL-33 has been shown to significantly impact allergic diseases, primarily by inducing Th2 immune responses. IL-33 is a key regulator of mast cell function and a promising therapeutic target for treating allergic diseases. This review provides an overview of the current understanding of the role of IL-33 in allergy pathogenesis and potential clinical approaches.

白细胞介素-33在变应性疾病发病和治疗中的生物学机制及治疗前景。
过敏性疾病严重影响着世界各地人们的生活质量。细胞因子在调节免疫系统中起着至关重要的作用。由于它们在促炎机制中的重要性,细胞因子被用来了解许多疾病的发病机制和作为生物标志物。其中一种细胞因子是白细胞介素-33,它是IL-1家族的成员,包括IL- 1α、IL-1β和IL-18。IL-33受体是IL-1受体样1和IL-1受体辅助蛋白的异源二聚体。IL-33在调节先天和适应性免疫应答中起关键作用。IL-33在体内的主要靶点是组织驻留免疫细胞,包括肥大细胞、2组先天淋巴样细胞、调节性T细胞、辅助性T细胞、嗜酸性粒细胞、嗜碱性粒细胞、树突状细胞、Th1细胞、CD8 + T细胞、NK细胞、iNKT细胞、B细胞、中性粒细胞和巨噬细胞。然而,IL-33似乎作为一个警报信号,在细胞损伤或应激条件下产生的细胞迅速释放。IL-33调节信号和各种生物功能,包括诱导促炎细胞因子、调节细胞增殖和参与组织重塑。IL-33是免疫相关疾病的基础,在炎症控制中起关键作用。最近,IL-33已被证明主要通过诱导Th2免疫反应显著影响过敏性疾病。IL-33是肥大细胞功能的关键调节因子,是治疗过敏性疾病的有希望的治疗靶点。本文综述了目前对IL-33在过敏发病机制中的作用和潜在的临床方法的理解。
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来源期刊
CiteScore
7.90
自引率
0.00%
发文量
18
审稿时长
>12 weeks
期刊介绍: Journal of Inflammation welcomes research submissions on all aspects of inflammation. The five classical symptoms of inflammation, namely redness (rubor), swelling (tumour), heat (calor), pain (dolor) and loss of function (functio laesa), are only part of the story. The term inflammation is taken to include the full range of underlying cellular and molecular mechanisms involved, not only in the production of the inflammatory responses but, more importantly in clinical terms, in the healing process as well. Thus the journal covers molecular, cellular, animal and clinical studies, and related aspects of pharmacology, such as anti-inflammatory drug development, trials and therapeutic developments. It also considers publication of negative findings. Journal of Inflammation aims to become the leading online journal on inflammation and, as online journals replace printed ones over the next decade, the main open access inflammation journal. Open access guarantees a larger audience, and thus impact, than any restricted access equivalent, and increasingly so, as the escalating costs of printed journals puts them outside University budgets. The unrestricted access to research findings in inflammation aids in promoting dynamic and productive dialogue between industrial and academic members of the inflammation research community, which plays such an important part in the development of future generations of anti-inflammatory therapies.
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