导致1型糖尿病的炎症路径在怀孕期间开始
Angelica P Ahrens1, Raquel Dias1, Tuulia Hyötyläinen2
1Department of Microbiology and Cell Science, Institute of Food and Agricultural Sciences, University of Florida, Gainesville, FL, USA.
Nature communications
|January 7, 2026
概括
生命早期的炎症和出生时的环境毒素可以在诊断前几年预测1型糖尿病 (T1D) 的风险. 识别这些早期生物标志物为T1D预防策略提供了一个新的窗口.
科学领域:
- 免疫学 免疫学 免疫学
- 代谢学 代谢学 代谢学
- 环境健康 环境健康
背景情况:
- 全球1型糖尿病 (T1D) 发病率正在上升,但早期的生物学风险因素仍然不清楚.
- 了解早期决定因素对于制定T1D有效预防策略至关重要.
- 基于人口的出生队列研究对于识别预诊断风险因素至关重要.
研究的目的:
- 在一般人群中确定1型糖尿病 (T1D) 的早期生物风险因素.
- 调查出生时的炎症和代谢特征,预测未来的T1D诊断.
- 探索环境毒素在T1D发展中的作用.
主要方法:
- 利用瑞典人口基的ABIS出生队列 (n=16,683).
- 在新生儿血液样本 (286个对照组,146个病例) 上进行了Olink蛋白质组分析.
- 采用机器学习算法来识别T1D的预测性蛋白质子集.
主要成果:
- 在出生时确定与中性粒细胞迁移,细胞毒性和免疫调节有关的差异性蛋白质丰度.
- 尽管考虑了家族病史和其他因素,但几个蛋白质标记仍然是重要的预测因素.
- 与代谢产物 (牛油酸,氨酸,谷氨酸) 和有毒物质 (PFOS) 的确定的关联.
- 一个蛋白质子集准确预测T1D (AUC=0.89±0.02),独立于HLA遗传风险.
结论:
- 天生的免疫和组织重塑途径在出生时受到干扰,这些人后来发展为T1D.
- 早期的生命中断,包括环境暴露,可能表明β细胞的脆弱性.
- 在出生时对这些早期障碍的非侵入性识别为T1D在自身免疫性攻击之前的预防提供了机会.
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