新型抑制性细胞因子IL-35与支气管哮喘的研究进展

doi:10.12092/j.issn.1009-2501.2018.02.021

摘要/Abstract

摘要：

支气管哮喘（以下简称哮喘）是最常见的慢性呼吸系统疾病，它是遗传与环境等多因素参与的慢性气道炎症性疾病，迄今为止其发病机制尚不完全清楚。经典理论认为辅助T细胞Th1/Th2失衡，以产生γ干扰素（IFN-γ）为标志的Th1反应低下，免疫反应向Th2型反应偏斜，进而导致变应原特异的IgE增加和气道嗜酸粒细胞（EOS）浸润，以及气道慢性炎症和气道高反应性（AHR）。随着研究的不断深入，特别是调节性T细胞(Tregs)、辅助T细胞-17（Th17）的发现拓宽了人们对哮喘炎症机制的理解，哮喘炎症的发病机制不再局限于Th1/Th2模式。既往研究发现白介素12（IL-12），能有效增强调节性T细胞（Tregs）亚群的功能，而白介素35（IL-35）作为IL-12家族新的一员，同样可以增强Treg的免疫抑制功能，且有效抑制Th17细胞的增殖分化，抑制机体过度的免疫反应，阻止炎症对机体的免疫损伤，从而参与到哮喘的发病和调节，进而可能起保护性作用，本文主要综述IL-35的生物学特性及其在哮喘发生、发展中的作用。

关键词: 白介素35, 哮喘, 调节性T细胞, 辅助T细胞-17

Abstract:

Asthma, while its pathogenesis remains unclear, is the most common chronic respiratory disease influenced by many factors including genetic and environmental influences. Classical theories believe that T helper cells(Th)1/Th2 cells are unbalanced, which further decrease Th1 cells response, and increase Th2 cells response. They cause allergen specific IgE secretion, airway eosinophils (EOS) infiltration, chronic airway inflammation and airway hyper-responsiveness (AHR). The findings of regulatory T cells (Tregs) and Th17 renew the understanding of the inflammatory mechanisms of asthma. The pathogenesis is no longer confined to the Th1/Th2 model. Like interleukin 12(IL-12), interleukin 35（IL-35）which belongs to the IL-12 family can effectively enhance the function of the Tregs and inhibit the proliferation and differentiation of Th17 cells, the excessive immune response, and immune damage to the body.It can be concluded that IL-35 could be involved and may play a protective role in the pathogenesis and regulation of asthma through a variety of pathways. This review introduces the biological characteristics of IL-35 and its role in the development and pathogenesis of asthma.

Key words: IL-35, asthma, Tregs, Th17

中图分类号:

R562.2

吕平，彭万胜，董淮富. 新型抑制性细胞因子IL-35与支气管哮喘的研究进展[J]. 中国临床药理学与治疗学, 2018, 23(2): 230-234.

LV Ping, PENG Wansheng, DONG Huaifu. Research progress of the association between new inhibitory cytokines il-35 and bronchial asthma[J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2018, 23(2): 230-234.

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