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环境因素在自身免疫中的复杂作用:应激,一种非传染性环境因素,打破病毒潜伏状态,是病毒成为引发自身免疫性疾病的传染性环境因素之前的固有前提。

The mosaic of environment involvement in autoimmunity: the abrogation of viral latency by stress, a non-infectious environmental agent, is an intrinsic prerequisite prelude before viruses can rank as infectious environmental agents that trigger autoimmune diseases.

机构信息

Institute of Endocrinology and Diabetes, The Children's Hospital at Westmead, Sydney, NSW, Australia.

出版信息

Autoimmun Rev. 2014 Jun;13(6):635-40. doi: 10.1016/j.autrev.2013.12.003. Epub 2014 Jan 11.

Abstract

An autoimmune disease (AD), organ-specific or systemic, results from an aberrant response in which the protective immune system normally schooled to recognize and destroy invading infectious agents (viruses, etc.) instead fails to distinguish self-antigens and proceeds to attack and destroy the host's organs. There can be familial aggregation in which a single AD may occur in members of a family, or a single family may be afflicted with multiple ADs. Finally, sometimes multiple ADs co-occur in a single individual: the kaleidoscope of autoimmunity. Autoimmunity is a multifactorial process in which genetic, hormonal, immunological and environmental factors act in concert to materialize the mosaic of autoimmunity phenomenon. A genetically primed individual may yet not develop an AD: the contribution by an environmental factor (non-infectious or infectious) is essential for completion of the act. Of the non-infectious factors, stress plays a determinative step in autoimmunity in that it abrogates viral latency and thereby ordains the viruses to qualify as infectious environmental factors that trigger ADs. This is note-worthy as viruses rank first as the most important environmental triggers of ADs. Furthermore, all these viruses experience going through latency. Hence the hypothesis: "The abrogation of viral latency by stress, a non-infectious environmental agent, is an intrinsic prerequisite prelude before viruses can rank as infectious environmental agents that trigger autoimmune diseases". There is collaboration here between non-infectious- and infectious-agent to achieve the cause of autoimmunity. We say viral latency and stress have a covenant: continued perpetration of autoimmunity is dependent on the intervention by stress to reactivate latent infections.

摘要

自身免疫性疾病(AD)是一种器官特异性或全身性疾病,是由于保护免疫系统异常反应引起的,正常情况下,免疫系统能够识别和摧毁入侵的传染性病原体(病毒等),但在自身免疫性疾病中,免疫系统无法区分自身抗原,进而攻击和破坏宿主的器官。在某些情况下,单一的 AD 可能会在家族成员中出现,即家族聚集性 AD,或者一个家族可能会受到多种 AD 的影响。最后,有时单一个体中会同时出现多种 AD,即自身免疫的万花筒现象。自身免疫是一个多因素过程,遗传、激素、免疫和环境因素协同作用,共同导致自身免疫现象的马赛克出现。具有遗传倾向的个体可能仍不会发展为 AD:环境因素(非传染性或传染性)的贡献对于完成这一过程至关重要。在非传染性因素中,压力在自身免疫中起着决定性的作用,因为它会破坏病毒潜伏期,从而使病毒成为触发 AD 的传染性环境因素。这一点值得注意,因为病毒是 AD 最重要的环境触发因素之一。此外,所有这些病毒都经历潜伏期。因此,我们提出了这样一个假设:“压力(一种非传染性环境因素)破坏病毒潜伏期,是病毒成为触发自身免疫性疾病的传染性环境因素的内在先决条件”。非传染性和传染性因素在这里协同作用,导致自身免疫的发生。我们说病毒潜伏期和压力之间存在着一种约定:持续的自身免疫依赖于压力的干预来重新激活潜伏感染。

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