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在性结肠炎期间对人类结肠进行细胞内和细胞间的重新连接
Christopher S Smillie1, Moshe Biton2, Jose Ordovas-Montanes3
1Klarman Cell Observatory, Broad Institute, Cambridge, MA, USA.
Cell
|July 27, 2019
概括
这项研究将性结肠炎 (UC) 风险基因映射到结肠中的特定细胞类型. 它确定了参与UC病变和抗TNF治疗的新细胞子集和途径.
科学领域:
- 胃肠病学
- 免疫学
- 遗传学
背景情况:
- 全基因组关联研究 (GWAS) 已经确定了性结肠炎 (UC) 的众多危险基因.
- 细胞和分子机制的UC致病性仍然不完全理解.
- 细胞类型特异性的UC风险基因功能在很大程度上是未知的.
研究的目的:
- 创建一个全面的UC结肠粘膜单细胞地图.
- 确定与UC风险等位基因相关的细胞类型和途径.
- 研究UC中抗TNF治疗的耐药性机制.
主要方法:
- 来自UC患者和健康对照者的366, 650个细胞的单细胞RNA测序 (scRNA-seq).
- 生物信息分析以识别不同的细胞子集和基因表达模式.
- 将scRNA-seq数据与GWAS发现整合起来,以映射风险变异.
主要成果:
- 鉴定了51个上皮细胞,层细胞和免疫细胞子集,包括新型BEST4+肠细胞,微状细胞和IL13RA2+IL11+炎症纤维细胞.
- 特定细胞类型 (炎性纤维细胞,单细胞,T细胞) 与疾病扩散和细胞间通信枢纽的关联.
- 将许多UC风险基因映射到特定的细胞类型和共同调节的基因模块中,表明途径的融合.
- 鉴定可能与抗TNF治疗耐药性相关的炎性纤维细胞.
结论:
- 性结肠炎的发病涉及特定的细胞类型和途径,风险基因效应的趋同.
- 生成的细胞图谱为了解UC遗传风险和疾病机制提供了框架.
- 新型细胞子集及其功能为UC治疗提供了新的点.
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