The immunomodulatory of interleukin-33 in rheumatoid arthritis: A systematic review

IF 4.5 3区 医学 Q2 IMMUNOLOGY Clinical immunology Pub Date : 2024-05-31 DOI:10.1016/j.clim.2024.110264
Renli Liu, Fangfang Wang, Xing Luo, Fengfan Yang, Jie Gao, Haomiao Shen, Zhaohui Zheng
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Abstract

Rheumatoid arthritis (RA) is a systemic chronic autoimmune disease that primarily affects the joints and surrounding soft tissues, characterized by chronic inflammation and proliferation of the synovium. Various immune cells are involved in the pathophysiology of RA. The complex interplay of factors such as chronic inflammation, genetic susceptibility, dysregulation of serum antibody levels, among others, contribute to the complexity of the disease mechanism, disease activity, and treatment of RA. Recently, the cytokine storm leading to increased disease activity in RA has gained significant attention. Interleukin-33 (IL-33), a member of the IL-1 family, plays a crucial role in inflammation and immune regulation. ST2 (suppression of tumorigenicity 2 receptor), the receptor for IL-33, is widely expressed on the surface of various immune cells. When IL-33 binds to its receptor ST2, it activates downstream signaling pathways to exert immunoregulatory effects. In RA, IL-33 regulates the progression of the disease by modulating immune cells such as circulating monocytes, tissue-resident macrophages, synovial fibroblasts, mast cells, dendritic cells, neutrophils, T cells, B cells, endothelial cells, and others. We have summarized and analyzed these findings to elucidate the pathways through which IL-33 regulates RA. Furthermore, IL-33 has been detected in the synovium, serum, and synovial fluid of RA patients. Due to inconsistent research results, we conducted a meta-analysis on the association between serum IL-33, synovial fluid IL-33, and the risk of developing RA in patients. The pooled SMD was 1.29 (95% CI: 1.15–1.44), indicating that IL-33 promotes the onset and pathophysiological progression of RA. Therefore, IL-33 may serve as a biomarker for predicting the risk of developing RA and treatment outcomes. As existing drugs for RA still cannot address drug resistance in some patients, new therapeutic approaches are needed to alleviate the significant burden on RA patients and healthcare systems. In light of this, we analyzed the potential of targeting the IL-33/ST2-related signaling pathway to modulate immune cells associated with RA and alleviate inflammation. We also reviewed IL-33 and RA susceptibility-related single nucleotide polymorphisms, suggesting potential involvement of IL-33 and macrophage-related drug-resistant genes in RA resistance therapy. Our review elucidates the role of IL-33 in the pathophysiology of RA, offering new insights for the treatment of RA.

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白细胞介素-33 对类风湿性关节炎的免疫调节作用:系统综述。
类风湿性关节炎(RA)是一种全身性慢性自身免疫性疾病,主要影响关节和周围软组织,以滑膜的慢性炎症和增生为特征。各种免疫细胞参与了 RA 的病理生理学过程。慢性炎症、遗传易感性、血清抗体水平失调等因素的复杂相互作用,导致了 RA 的发病机制、疾病活动和治疗的复杂性。最近,导致 RA 疾病活动性增加的细胞因子风暴引起了广泛关注。白细胞介素-33(IL-33)是 IL-1 家族的成员之一,在炎症和免疫调节中发挥着至关重要的作用。IL-33的受体ST2(抑制肿瘤生成2受体)广泛表达于各种免疫细胞表面。当 IL-33 与其受体 ST2 结合时,会激活下游信号通路,从而发挥免疫调节作用。在 RA 中,IL-33 通过调节循环单核细胞、组织驻留巨噬细胞、滑膜成纤维细胞、肥大细胞、树突状细胞、中性粒细胞、T 细胞、B 细胞、内皮细胞等免疫细胞来调节疾病的进展。我们对这些发现进行了总结和分析,以阐明IL-33调节RA的途径。此外,在 RA 患者的滑膜、血清和滑液中也检测到了 IL-33。由于研究结果不一致,我们对血清IL-33、滑膜液IL-33与患者罹患RA风险之间的关系进行了荟萃分析。汇总的SMD为1.29(95% CI:1.15-1.44),表明IL-33会促进RA的发病和病理生理进展。因此,IL-33 可作为预测 RA 发病风险和治疗效果的生物标志物。由于现有的 RA 药物仍无法解决部分患者的耐药性问题,因此需要新的治疗方法来减轻 RA 患者和医疗系统的沉重负担。有鉴于此,我们分析了靶向 IL-33/ST2 相关信号通路以调节与 RA 相关的免疫细胞并缓解炎症的潜力。我们还回顾了IL-33和RA易感性相关的单核苷酸多态性,表明IL-33和巨噬细胞相关耐药基因可能参与RA耐药治疗。我们的综述阐明了IL-33在RA病理生理学中的作用,为RA的治疗提供了新的见解。
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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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