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矽肺与自身免疫

Silicosis and autoimmunity.

作者信息

Lee Suni, Hayashi Hiroaki, Mastuzaki Hidenori, Kumagai-Takei Naoko, Otsuki Takemi

机构信息

aDepartment of Hygiene bDepartment of Dermatology, Kawasaki Medical School, Kurashiki, Okayama, Japan.

出版信息

Curr Opin Allergy Clin Immunol. 2017 Apr;17(2):78-84. doi: 10.1097/ACI.0000000000000350.

Abstract

PURPOSE OF REVIEW

Of the various environmental, occupational, and medical substances that cause dysregulation of autoimmunity, the effects and causative mechanisms of silica particles and asbestos fibers are discussed in this review.

RECENT FINDINGS

With respect to silica, many epidemiological studies have shown a significant association between silica exposure and the occurrence of autoimmune diseases. Although the importance of the NACHT, LRR and PYD domains-containing protein 3 (NALP3) inflammasome as the initial immune reaction against silica particles has been identified, the mechanisms involved that lead to various autoimmune diseases in patients exposed to silica remain largely unknown. Silica can activate various immune cells and investigation of the associated imbalance of regulatory T cells, responder T cells as well as Th17 cells might be key in furthering our understanding of silica-induced autoimmune alterations. On the other hand, asbestos exposure shows less association with autoimmune diseases. However, interesting findings pertaining to the detection of antiendothelial and mesothelial cell antibodies in asbestos-exposed patients have been reported.

SUMMARY

Taken together, further investigations may contribute in delineating the mechanisms involved in environmental factor-induced modification of autoimmunity.

摘要

综述目的

在各种导致自身免疫失调的环境、职业和医学物质中,本文综述了二氧化硅颗粒和石棉纤维的影响及致病机制。

最新发现

关于二氧化硅,许多流行病学研究表明二氧化硅暴露与自身免疫性疾病的发生之间存在显著关联。尽管含NACHT、LRR和PYD结构域的蛋白3(NALP3)炎性小体作为针对二氧化硅颗粒的初始免疫反应的重要性已得到确认,但导致接触二氧化硅的患者发生各种自身免疫性疾病的相关机制仍 largely未知。二氧化硅可激活各种免疫细胞,研究调节性T细胞、反应性T细胞以及Th17细胞的相关失衡可能是进一步了解二氧化硅诱导的自身免疫改变的关键。另一方面,石棉暴露与自身免疫性疾病的关联较小。然而,已报道了在石棉暴露患者中检测到抗内皮细胞和间皮细胞抗体的有趣发现。

总结

综上所述,进一步的研究可能有助于阐明环境因素诱导自身免疫改变所涉及的机制。

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