Epidemiology of environmental exposures and human autoimmune diseases: findings from a National Institute of Environmental Health Sciences Expert Panel Workshop.

Epidemiology of environmental exposures and human autoimmune diseases: findings from a National Institute of Environmental Health Sciences Expert Panel Workshop.
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DOI:
10.1016/j.jaut.2012.05.002
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发表时间:
2012-12
影响因子:
12.8
通讯作者:
De Roos AJ
De Roos AJ
中科院分区:
医学1区
文献类型:
--
作者:
Miller FW;Alfredsson L;Costenbader KH;Kamen DL;Nelson LM;Norris JM;De Roos AJ

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自身免疫性疾病(AID)是许多病因不明的复杂疾病的集合,其导致对自身抗原的免疫应答,并且被认为是由遗传和环境因素之间的相互作用引起的。在这里,我们审查的流行病学证据的作用,环境因素在人类艾滋病的发展,结论,可以从现有的数据,关键的知识差距,研究需要填补这些空白,解决不确定性。我们特别总结了知识的状态和我们的信心水平在特定的代理人在自身免疫性疾病的发展中的作用,我们定义了未来调查的影响最大的领域。在我们的共识发现中,我们确信:1)结晶二氧化硅暴露可促进几种AID的发展; 2)溶剂暴露可促进系统性硬化症的发展; 3)吸烟可促进血清阳性类风湿性关节炎的发展;以及4)紫外线辐射暴露与多发性硬化症发展风险之间存在负相关。我们建议需要更多的表型,基因型和多重暴露的研究。需要调查的其他知识差距包括:确定与年龄、发育状态和激素变化有关的暴露和延迟时间的重要窗口;了解剂量-反应关系;阐明疾病发展的机制。解决这些基本问题将需要更多的资源来支持研究,特别是对罕见艾滋病的研究,但了解特定遗传背景下环境因素带来的风险可能为今后预防艾滋病铺平道路。
Autoimmune diseases (AID) are a collection of many complex disorders of unknown etiology resulting in immune responses to self-antigens and are thought to result from interactions between genetic and environmental factors. Here we review the epidemiologic evidence for the role of environmental factors in the development of human AID, the conclusions that can be drawn from the existing data, critical knowledge gaps, and research needed to fill these gaps and to resolve uncertainties. We specifically summarize the state of knowledge and our levels of confidence in the role of specific agents in the development of autoimmune diseases, and we define the areas of greatest impact for future investigations. Among our consensus findings we are confident that: 1) crystalline silica exposure can contribute to the development of several AID; 2) solvent exposure can contribute to the development of systemic sclerosis; 3) smoking can contribute to the development of seropositive rheumatoid arthritis; and 4) an inverse association exists between ultraviolet radiation exposure and the risk of development of multiple sclerosis. We suggest that more studies of phenotypes, genotypes, and multiple exposures are needed. Additional knowledge gaps needing investigation include: defining important windows in the timing of exposures and latencies relating to age, developmental state, and hormonal changes; understanding dose-response relationships; and elucidating mechanisms for disease development. Addressing these essential issues will require more resources to support research, particularly of rare AID, but knowledge of the risks conferred by environmental factors in specific genetic contexts could pave the way for prevention of AID in the future.
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