Using single-cell technologies to map the human immune system — implications for nephrology

免疫系统 医学 肾病科 细胞 免疫学 质量细胞仪 电池类型 计算生物学 生物 内科学 基因 表型 遗传学
作者
Benjamin J. Stewart,John R. Ferdinand,Menna R. Clatworthy
出处
期刊:Nature Reviews Nephrology [Nature Portfolio]
卷期号:16 (2): 112-128 被引量:62
标识
DOI:10.1038/s41581-019-0227-3
摘要

Advances in single-cell technologies are transforming our understanding of cellular identity. For instance, the application of single-cell RNA sequencing and mass cytometry technologies to the study of immune cell populations in blood, secondary lymphoid organs and the renal tract is helping researchers to map the complex immune landscape within the kidney, define cell ontogeny and understand the relationship of kidney-resident immune cells with their circulating counterparts. These studies also provide insights into the interactions of immune cell populations with neighbouring epithelial and endothelial cells in health, and across a range of kidney diseases and cancer. These data have translational potential and will aid the identification of drug targets and enable better prediction of off-target effects. The application of single-cell technologies to clinical renal biopsy samples, or even cells within urine, will improve diagnostic accuracy and assist with personalized prognostication for patients with various kidney diseases. A comparison of immune cell types in peripheral blood and secondary lymphoid organs in healthy individuals and in patients with systemic autoimmune diseases that affect the kidney will also help to unravel the mechanisms that underpin the breakdown in self-tolerance and propagation of autoimmune responses. Together, these immune cell atlases have the potential to transform nephrology. In this Review, Stewart and colleagues describe how single-cell technologies, in particular single-cell RNA sequencing, can be used to map the complex immune landscape within organs, and how such technologies might provide insights into the role of the immune system in kidney health and disease pathogenesis.
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