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[环境与自身免疫——从外部病因到内在冲突]

[The environment and autoimmunity--from external causes to inner conflicts].

作者信息

Gebbers J O

机构信息

Pathologisches Institut, Kantonsspital Luzern.

出版信息

Praxis (Bern 1994). 2001 Nov 1;90(44):1913-22.

Abstract

Autoimmune disorders result from a breakdown of immunologic tolerance leading to an immune response against self-molecules. In most instances the events that initiate the immune response to self-molecules are unknown, but a number of studies suggest associations with environmental and genetic factors and certain types of infections. The concordance of autoimmune diseases among identical twins is virtually always less than 50%, often in the 25-40% range. This observation, as well as epidemic clustering of some autoimmune diseases following xenobiotic exposure, reinforces the thesis that autoimmune disease is secondary to both genetic and environmental factors. In addition, because of individual genetic susceptibilities based not only on major histocompatibility complex differences but also on differences in toxin metabolism, lifestyles, and exposure rates, individuals will react differently to the same chemicals. With these comments in mind it is important to note that there have been associations of a number of xenobiotics with human autoimmune disease, including mercury, iodine, vinyl chloride, canavanine, organic solvents, silica, L-tryptophan, particulates, ultraviolet radiation, and ozone. In addition, there is discussion in the literature that raises the possibility that xenobiotics may also exacerbate an existing autoimmune disorder. In this article these issues are discussed, in particular, the evidence for the role of environmental agents in the initiation or progression of autoimmune conditions. With the worldwide deterioration of the environment, this is a particular important subject for human health. This is best illustrated by the epidemics of eosinophilic myalgia syndrome with shared characteristics that occurred about 20 years ago. Another example is the toxic oil syndrome of Spain in 1981 involving cooking oil led to both acute and chronic disease as well as formation of auto-antibodies to collagen, DNA, and skeletal muscle. Currently the question is risen whether there is a link between environmental estrogens and autoimmune disorders, especially since these illnesses are reported possibly more frequent. Yet for the time being, an answer is not available, since the current state of science with respect to autoimmunity and environmental agents is still in the early stages of hazard identification.

摘要

自身免疫性疾病是由于免疫耐受的破坏,导致机体对自身分子产生免疫反应。在大多数情况下,引发针对自身分子免疫反应的事件尚不清楚,但一些研究表明,这与环境和遗传因素以及某些类型的感染有关。同卵双胞胎中自身免疫性疾病的一致性几乎总是低于50%,通常在25%-40%的范围内。这一观察结果,以及一些自身免疫性疾病在接触外源性物质后出现的流行聚集现象,强化了自身免疫性疾病是遗传和环境因素共同作用的结果这一论点。此外,由于个体的遗传易感性不仅基于主要组织相容性复合体的差异,还基于毒素代谢、生活方式和接触率的差异,个体对相同化学物质的反应会有所不同。考虑到这些情况,需要注意的是,许多外源性物质与人类自身免疫性疾病有关,包括汞、碘、氯乙烯、刀豆氨酸、有机溶剂、二氧化硅、L-色氨酸、颗粒物、紫外线辐射和臭氧。此外,文献中也有讨论提出,外源性物质可能还会加重现有的自身免疫性疾病。在本文中,将对这些问题进行讨论,特别是环境因素在自身免疫性疾病的引发或进展中所起作用的证据。随着全球环境的恶化,这对人类健康来说是一个尤为重要的课题。大约20年前发生的具有共同特征的嗜酸性肌痛综合征疫情就是最好的例证。另一个例子是1981年西班牙发生的有毒食用油综合征,涉及食用油,导致了急性和慢性疾病,以及针对胶原蛋白、DNA和骨骼肌的自身抗体的形成。目前,人们提出了环境雌激素与自身免疫性疾病之间是否存在联系的问题,特别是因为据报道这些疾病可能更为常见。然而,目前还没有答案,因为关于自身免疫和环境因素的科学研究仍处于危害识别的早期阶段。

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