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控制过敏反应的变应原编码信号。

Allergen-encoded signals that control allergic responses.

作者信息

Tung Hui-Ying, Landers Cameron, Li Evan, Porter Paul, Kheradmand Farrah, Corry David B

机构信息

aDepartment of Pathology & Immunology bTranslational Biology and Molecular Medicine Program cDepartment of Medicine dBiology of Inflammation Center, Baylor College of Medicine eMichael E. DeBakey VA Center for Translational Research on Inflammatory Diseases, Houston, Texas, USA.

出版信息

Curr Opin Allergy Clin Immunol. 2016 Feb;16(1):51-8. doi: 10.1097/ACI.0000000000000233.

DOI:10.1097/ACI.0000000000000233
PMID:26658015
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4863991/
Abstract

PURPOSE OF REVIEW

The purpose is to review the important recent advances made in how innate immune cells, microbes, and the environment contribute to the expression of allergic disease, emphasizing the allergen-related signals that drive allergic responses.

RECENT FINDINGS

The last few years have seen crucial advances in how innate immune cells such as innate lymphoid cells group 2 and airway epithelial cells and related molecular pathways through organismal proteinases and innate immune cytokines, such as thymic stromal lymphopoietin, IL-25, and IL-33 contribute to allergy and asthma. Simultaneously with these advances, important progress has been made in our understanding of how the environment, and especially pathogenic organisms, such as bacteria, viruses, helminths, and especially fungi derived from the natural and built environments, either promote or inhibit allergic inflammation and disease. Of specific interest are how lipopolysaccharide mediates its antiallergic effect through the ubiquitin modifying factor A20 and the antiallergic activity of both helminths and protozoa.

SUMMARY

Innate immune cells and molecular pathways, often activated by allergen-derived proteinases acting on airway epithelium and macrophages as well as additional unknown factors, are essential to the expression of allergic inflammation and disease. These findings suggest numerous future research opportunities and new opportunities for therapeutic intervention in allergic disease.

摘要

综述目的

旨在回顾近期在固有免疫细胞、微生物和环境如何促成过敏性疾病表达方面取得的重要进展,重点关注驱动过敏反应的过敏原相关信号。

近期发现

过去几年,在固有淋巴细胞2组和气道上皮细胞等固有免疫细胞以及通过机体蛋白酶和固有免疫细胞因子(如胸腺基质淋巴细胞生成素、白细胞介素-25和白细胞介素-33)的相关分子途径如何促成过敏和哮喘方面取得了关键进展。与此同时,在我们对环境,尤其是来自自然和人造环境的细菌、病毒、蠕虫,特别是真菌等致病生物如何促进或抑制过敏性炎症和疾病的理解上也取得了重要进展。特别值得关注的是脂多糖如何通过泛素修饰因子A20介导其抗过敏作用以及蠕虫和原生动物的抗过敏活性。

总结

固有免疫细胞和分子途径通常由作用于气道上皮和巨噬细胞的过敏原衍生蛋白酶以及其他未知因素激活,对于过敏性炎症和疾病的表达至关重要。这些发现为过敏性疾病的未来研究和治疗干预带来了众多机会。

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Allergol Int. 2014;63(3):443-455. doi: 10.2332/allergolint.13-OA-0672. Epub 2015 Feb 27.
2
Farm dust and endotoxin protect against allergy through A20 induction in lung epithelial cells.农田尘螨和内毒素通过肺上皮细胞中 A20 的诱导来预防过敏。
Science. 2015 Sep 4;349(6252):1106-10. doi: 10.1126/science.aac6623.
3
The TLR4-associated phospholipase D1 activation is crucial for Der f 2-induced IL-13 production.TLR4 相关的磷脂酶 D1 的激活对于 Der f 2 诱导的 IL-13 产生至关重要。
Allergy. 2015 Dec;70(12):1569-79. doi: 10.1111/all.12764. Epub 2015 Sep 28.
4
Microbial Ligand Costimulation Drives Neutrophilic Steroid-Refractory Asthma.微生物配体共刺激驱动嗜中性粒细胞性类固醇难治性哮喘。
PLoS One. 2015 Aug 11;10(8):e0134219. doi: 10.1371/journal.pone.0134219. eCollection 2015.
5
Rho-kinase inhibitor fasudil reduces allergic airway inflammation and mucus hypersecretion by regulating STAT6 and NFκB.Rho激酶抑制剂法舒地尔通过调节信号转导和转录激活因子6(STAT6)及核因子κB(NFκB)来减轻过敏性气道炎症和黏液高分泌。
Clin Exp Allergy. 2015 Dec;45(12):1812-22. doi: 10.1111/cea.12606.
6
An Interleukin-33-Mast Cell-Interleukin-2 Axis Suppresses Papain-Induced Allergic Inflammation by Promoting Regulatory T Cell Numbers.白细胞介素-33-肥大细胞-白细胞介素-2轴通过增加调节性T细胞数量抑制木瓜蛋白酶诱导的过敏性炎症。
Immunity. 2015 Jul 21;43(1):175-86. doi: 10.1016/j.immuni.2015.06.021.
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