Immune checkpoint molecule TIGIT regulates kidney T cell functions and mediates acute kidney injury

This dataset includes the single cell RNA-seq data associated with the publication listed in the title (abstract below). CellRanger.zip contains the raw transcript counts as produced by CellRanger. There is one folder per sample. The samples are indicated by the folder name (e.g. KO_Ctrl). We have also included .h5ad files that contain of cells that passed quality control, as described in the manuscript. adTIGIT_raw_031422.h5ad contains all passing cells and the raw counts, as well as cell annotations ('celltype') adTIGIT_Tonly_091421.h5ad contains only T cells, .X contains the normalized data and T-cell sub-type ('cluster'). Abstract: T cells mediate pathologic and reparative processes during acute kidney injury (AKI) but exact mechanisms regulating kidney T cell functions are unclear. This study identified upregulation of the novel immune checkpoint molecule, TIGIT, on mouse and human kidney T cells following AKI. TIGIT-expressing kidney T cells produced proinflammatory cytokines and had effector and central memory phenotype. Kidney Tregs were predominantly TIGIT+ and reduced after ischemia reperfusion (IR) injury. TIGIT deficient mice had protection from both ischemic and nephrotoxic AKI. Single cell RNA sequencing led to discovery of possible downstream targets of TIGIT. TIGIT mediates AKI pathophysiology, is a promising target for developing AKI therapy, and is being increasingly studied in human cancer therapy trials