泌尿系统膜性肾病的免疫反应概述:关注细胞因子和治疗方案。

IF 1.9 4区 医学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY
Chao Luo, Chengcheng Wei, Zhaoxian He, Renlei Feng
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引用次数: 0

摘要

膜性肾病(MN)是一种自身免疫性疾病,是由于免疫细胞缺乏自身耐受机制而产生针对肾小球荚膜抗原的自身抗体所致。与许多自身免疫性疾病类似,MN 的发病机理至今仍很模糊,人们正在进行许多实验来检测 MN 的抗原和遗传原因。最近,在不存在抗磷脂酶 A2 受体抗原的 MN 患者中发现了新的抗原,如外显子素 1/外显子素 2、神经 EGF 样-1、semaphorin 3B 和原粘连蛋白 7。此外,细胞因子是调节免疫反应的分子,已被发现在多种自身免疫性疾病中具有有害作用,包括多发性硬化症、类风湿性关节炎、系统性红斑狼疮和 MN。本文将讨论细胞因子在 MN 患者中的作用和治疗策略。随着人们对该疾病认识的加深,可能会开发出针对特定抗原或细胞因子的靶向疗法,以有效控制 MN。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Overview of Immunological Response in Urological Membranous Nephropathy: Focus on Cytokine and Treatment Options.

Membranous nephropathy (MN) is an autoimmune disease that is caused by the production of autoantibody against glomerular podocyte antigens by immune cells due to the lack of self-tolerance mechanisms. Similar to many autoimmune diseases, the pathogenesis of MN is still vague and many experiments are being conducted to detect the antigens and genetic reasons for MN illness. Recently, new antigens, such as exotosin 1/exotosin 2, neural EGF-like-1, semaphorin 3B, and protocadherin 7 have been identified in MN patients who did not have presence of antiphospholipase A2 receptor antigen. What is more, cytokines, which are molecules that regulate immune responses, have been found to have harmful effects in various autoimmune diseases, including multiple sclerosis, rheumatoid arthritis, systemic lupus erythematosus, and MN. The role of cytokines and treatment strategies in MN patients is discussed in this article. As the understanding of the disease improves, targeted therapies that focus on specific antigens or cytokines may be developed to effectively manage MN.

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来源期刊
CiteScore
3.80
自引率
0.00%
发文量
78
审稿时长
2.2 months
期刊介绍: Journal of Interferon & Cytokine Research (JICR) provides the latest groundbreaking research on all aspects of IFNs and cytokines. The Journal delivers current findings on emerging topics in this niche community, including the role of IFNs in the therapy of diseases such as multiple sclerosis, the understanding of the third class of IFNs, and the identification and function of IFN-inducible genes.
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