Single cell and spatial transcriptomics analysis of kidney double negative T lymphocytes in normal and ischemic mouse kidneys.
Single cell and spatial transcriptomics analysis of kidney double negative T lymphocytes in normal and ischemic mouse kidneys.
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DOI:
10.1038/s41598-023-48213-2
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发表时间:
2023-11-28
影响因子:
4.6
通讯作者:
中科院分区:
文献类型:
--
作者:
T cells are important in the pathogenesis of acute kidney injury (AKI), and TCR+CD4-CD8- (double negative-DN) are T cells that have regulatory properties. However, there is limited information on DN T cells compared to traditional CD4+ and CD8+ cells. To elucidate the molecular signature and spatial dynamics of DN T cells during AKI, we performed single-cell RNA sequencing (scRNA-seq) on sorted murine DN, CD4+, and CD8+ cells combined with spatial transcriptomic profiling of normal and post AKI mouse kidneys. scRNA-seq revealed distinct transcriptional profiles for DN, CD4+, and CD8+ T cells of mouse kidneys with enrichment of Kcnq5, Klrb1c, Fcer1g, and Klre1 expression in DN T cells compared to CD4+ and CD8+ T cells in normal kidney tissue. We validated the expression of these four genes in mouse kidney DN, CD4+ and CD8+ T cells using RT-PCR and Kcnq5, Klrb1, and Fcer1g genes with the NIH human kidney precision medicine project (KPMP). Spatial transcriptomics in normal and ischemic mouse kidney tissue showed a localized cluster of T cells in the outer medulla expressing DN T cell genes including Fcer1g. These results provide a template for future studies in DN T as well as CD4+ and CD8+ cells in normal and diseased kidneys.
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DOI:
10.1053/j.ajkd.2018.03.028
发表时间:
2018-12
期刊:
American journal of kidney diseases : the official journal of the National Kidney Foundation
影响因子:
--
作者:
Lee SA;Cozzi M;Bush EL;Rabb H
通讯作者:
Rabb H
影响因子:
12.4
作者:
Liu, Yongguang;Hu, Jianmin;Zhao, Ming
通讯作者:
Zhao, Ming
影响因子:
15.9
作者:
Burne, MJ;Daniels, F;Rabb, H
通讯作者:
Rabb, H
影响因子:
5.5
作者:
Ascon, Dolores B.;Ascon, Miguel;Rabb, Hamid
通讯作者:
Rabb, Hamid
影响因子:
9.2
作者:
Chen L;Yuan L;Wang Y;Wang G;Zhu Y;Cao R;Qian G;Xie C;Liu X;Xiao Y;Wang X
通讯作者:
Wang X