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调节性 T 细胞对 Th2 介导炎症的控制作用。

Control of Th2-mediated inflammation by regulatory T cells.

机构信息

Karmanos Cancer Institute and Department of Immunology and Microbiology, Wayne State University, Detroit, Michigan, USA.

出版信息

Am J Pathol. 2010 Aug;177(2):525-31. doi: 10.2353/ajpath.2010.090936. Epub 2010 Jun 21.

DOI:10.2353/ajpath.2010.090936
PMID:20566752
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2913351/
Abstract

Allergic diseases and asthma are caused by dysregulated Th2-type immune responses, which drive disease development in susceptible individuals. Immune tolerance to allergens prevents inflammatory symptoms in the respiratory mucosa and provides protection against inflammation in the airways. Increasing evidence indicates that Foxp3+ regulatory T cells (Tregs) play a critical role in immune tolerance and control Th2-biased responses. Tregs develop in the thymus from CD4(+) T cells (natural Tregs) and also in the periphery by the conversion of naïve CD4(+) T cells (induced Tregs). Increased susceptibility to allergy and airway inflammation is hypothesized to result from impaired development and function of Tregs. Thus, strategies to induce allergen-specific Tregs hold great promise for treatment and prevention of asthma.

摘要

过敏性疾病和哮喘是由 Th2 型免疫反应失调引起的,这种免疫反应会促使易感个体发生疾病。对过敏原的免疫耐受可防止呼吸道黏膜发生炎症症状,并可预防气道炎症。越来越多的证据表明,Foxp3+调节性 T 细胞(Treg)在免疫耐受和控制 Th2 偏向性反应中发挥着关键作用。Treg 从 CD4(+)T 细胞(天然 Treg)在胸腺中发育,也可从初始 CD4(+)T 细胞(诱导性 Treg)在外周发育。假设过敏和气道炎症的易感性增加是由于 Treg 的发育和功能受损所致。因此,诱导过敏原特异性 Treg 的策略有望成为治疗和预防哮喘的方法。

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本文引用的文献

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Cutting edge: CD28 and c-Rel-dependent pathways initiate regulatory T cell development.前沿:CD28 和 c-Rel 依赖性途径启动调节性 T 细胞的发育。
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