Beta 细胞活性与 1 型糖尿病的发展。

IF 2.2 4区 医学 Q4 IMMUNOLOGY
Apmis Pub Date : 2024-05-26 DOI:10.1111/apm.13441
Rikke Thea, Karsten Buschard
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引用次数: 0

摘要

1 型糖尿病(T1D)是一种自身免疫性疾病,会导致胰岛完整性降低和分泌胰岛素的贝塔细胞遭到破坏。在这篇综述中,我们研究了 T1D 的发展与 beta 细胞活性之间的内在关系。1982 年,人们最初假设,β 细胞活性的增加会增强表面抗原的表达,从而吸引免疫系统。后来,其他研究结果也支持这一观点,包括怀孕三个月时 T1D 发病风险增加,以及俄罗斯和芬兰卡累利阿地区因生活方式不同而导致 T1D 发病率不同。高β细胞活性的其他影响,如降低硫甙水平、形成不正确的胰岛素分子以及在病毒攻击时增加 IFN-α,都可能导致 T1D 的发生。预防 T1D 发生的一个可行方法是降低 beta 细胞的活性,这在动物模型中已显示出良好的效果。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Beta-cell activity and development of Type 1 diabetes.

Type 1 diabetes (T1D) is an autoimmune disease, resulting in diminished islet integrity and destruction of the insulin-secreting beta cells. In this review, we investigate the intrinsic relationship between the development of T1D and the activity of the beta cells. The idea was initially hypothesized in 1982 that an increased beta-cell activity would enhance the surface antigen expression and thereby attract the immune system. Later, other findings support this idea, including increased risk of T1D development during third trimester of pregnancy, and the difference in T1D incidence in Russian and Finnish Karelia due to different lifestyles. Other implications of high beta-cell activity, such as reduced sulfatide levels, formation of non-correct insulin molecules and an increase in IFN-alpha upon virus attack, can contribute to the development of T1D. A possible way to prevent the development of T1D is to diminish beta-cell activity, which has shown promising results in animal models.

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来源期刊
Apmis
Apmis 医学-病理学
CiteScore
5.20
自引率
0.00%
发文量
91
审稿时长
2 months
期刊介绍: APMIS, formerly Acta Pathologica, Microbiologica et Immunologica Scandinavica, has been published since 1924 by the Scandinavian Societies for Medical Microbiology and Pathology as a non-profit-making scientific journal.
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