在人类肥胖相关的元炎症中,线粒体采购干扰原体连接体和自身抗原
Amrit Raj Ghosh1, Purbita Bandopadhyay1,2, Jit Sarkar3
1Translational Research Unit of Excellence, CSIR-Indian Institute of Chemical Biology, Kolkata, India.
Obesity (Silver Spring, Md.)
|July 26, 2023
概括
线粒体DNA (mtDNA) 与内脏脂肪组织 (VAT) 中的TFAM蛋白结合,引发肥胖症的炎症. 这项研究确定了TFAM作为自身抗原的来源,为与肥胖相关的免疫机制提供了新的见解.
科学领域:
- 免疫学 免疫学 免疫学
- 代谢性疾病研究研究
- 线粒体生物学 线粒体生物学
背景情况:
- 内脏脂肪组织 (VAT) 炎症是与肥胖相关的代谢功能障碍的一个关键因素.
- 等离子体树突细胞 (pDCs) 被通用类受体9 (TLR9) 激活,识别自身DNA,启动I型干扰素的产生和VAT炎症.
研究的目的:
- 为了研究线粒体DNA (mtDNA) 在激活TLR9中的作用,在肥胖症中的VAT招募的pDC中.
- 为了识别促进mtDNA访问TLR9.9的蛋白质载体.
- 确定这种机制是否也会在肥胖的背景下产生自身抗原.
主要方法:
- 对来自肥胖和瘦身个体的增值税样本进行基因表达和脂肪显微培养的分析.
- 人类pDC培养物用脂肪开拓性超剂和随后的干扰素-α ELISA 的处理.
- 从肥胖和非肥胖个体的血样本中寻找自身抗体的ELISA.
主要成果:
- 在VAT中的线粒体DNA (mtDNA),与线粒体转录因子A (TFAM) 复合,作为肥胖症中pDCs的干扰因子连接体.
- 肥胖会诱导针对TFAM的幽默性自身免疫反应.
结论:
- 肥胖个体的VAT中功能障碍的线粒体可以产生干扰因子连接体和自身抗原.
- 肥胖的这种免疫路径对未来的治疗和预后策略有潜力.
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