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当前碘环境下的甲状腺自身免疫

Thyroid autoimmunity in the current iodine environment.

作者信息

Papanastasiou Labrini, Vatalas Ioannis-Anastasios, Koutras Demetrios A, Mastorakos George

机构信息

Endocrine Unit, Evgenidion Hospital, Athens University, Athens, Greece.

出版信息

Thyroid. 2007 Aug;17(8):729-39. doi: 10.1089/thy.2006.0299.

Abstract

Iodine is essential for thyroid function. Thyroid disorders related to iodine deficiency decreased progressively with the continuous iodine prophylaxis and the increased iodine intake. An adverse effect resulting from iodine prophylaxis may be the induction of thyroid autoimmunity. Although experiments performed in animal models suggest that iodine could initiate or exacerbate thyroid autoimmunity, the role of iodine in humans remains controversial. Several observational studies in areas with adequate or high iodine intake suggest that there is an increase in the incidence of thyroid autoimmune disease. Moreover, intervention studies suggest that increased iodine intake may enhance thyroid autoimmunity too. However, not all studies generated the same findings, probably because of genetic, racial, and environmental differences. It seems that autoimmune exacerbation is a transient phenomenon. Studies have shown that in persons presenting thyroid antibodies, the levels of these antibodies progressively decrease when the majority of them react against a nonspecific pattern of thyroglobulin (Tg) epitopes. However, in a small number of these persons, the anti-Tg antibodies are similar to those in patients with patent thyroid autoimmune disease, reacting against specific immunodominant Tg epitopes, and their levels persist. One possible attractive explanation is that enhanced iodine intake increases the antigenicity of Tg through the incorporation of iodine into its molecule and the formation of iodinated Tg epitopes or even the generation of noniodinated pathogenetic Tg epitopes that are normally cryptic.

摘要

碘对于甲状腺功能至关重要。随着持续的碘预防措施以及碘摄入量的增加,与碘缺乏相关的甲状腺疾病逐渐减少。碘预防可能产生的不良影响是诱发甲状腺自身免疫。尽管在动物模型中进行的实验表明碘可引发或加剧甲状腺自身免疫,但碘在人类中的作用仍存在争议。在碘摄入量充足或较高地区的多项观察性研究表明,甲状腺自身免疫性疾病的发病率有所增加。此外,干预性研究表明,碘摄入量增加也可能增强甲状腺自身免疫。然而,并非所有研究都得出相同的结果,这可能是由于遗传、种族和环境差异所致。似乎自身免疫加剧是一种短暂现象。研究表明,在出现甲状腺抗体的人群中,当大多数抗体针对甲状腺球蛋白(Tg)表位的非特异性模式发生反应时,这些抗体的水平会逐渐降低。然而,在少数这类人群中,抗Tg抗体与甲状腺自身免疫性疾病患者的抗体相似,针对特定的免疫显性Tg表位发生反应,且其水平持续存在。一种可能有吸引力的解释是,碘摄入量增加通过将碘掺入Tg分子并形成碘化Tg表位,甚至产生通常隐藏的非碘化致病性Tg表位,从而增加了Tg的抗原性。

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