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A human mutation in STAT3 promotes type 1 diabetes through a defect in CD8+ T cell tolerance [scRNA, scTCR]

ABSTRACT: scRNA-seq datasets of immune cells in K392R and WT mice

ORGANISM(S): Mus musculus

PROVIDER: GSE173413 | GEO | 2021/06/01

REPOSITORIES: GEO

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A human mutation in STAT3 promotes type 1 diabetes through a defect in CD8+ T cell tolerance [scATAC]

Project description:scATAC-seq datasets of immune cells in K392R and WT mice

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A human mutation in STAT3 promotes type 1 diabetes through a defect in CD8+ T cell tolerance [scRNA, scTCR]

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A human mutation in STAT3 promotes type 1 diabetes through a defect in CD8+ T cell tolerance

Project description:This SuperSeries is composed of the SubSeries listed below.

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A human mutation in STAT3 promotes type 1 diabetes through a defect in CD8+ T cell tolerance

Project description:A human mutation in STAT3 promotes type 1 diabetes through a defect in CD8+ T cell tolerance

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scRNA-seq and scTCR-seq of tetramer-positive T cells from IL27 treated tumor bearing mice

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A human mutation in STAT3 promotes type 1 diabetes through a defect in CD8+ T cell tolerance [scATAC]

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Mouse pancreatic islet scRNA-seq atlas across sexes, ages, and stress conditions including diabetes

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scRNA-seq and scTCR-seq of autoreactive CD8 T cells from NOD mice

Project description:Type 1 diabetes (T1D) is an autoimmune disorder defined by CD8 T cell-mediated destruction of pancreatic β cells. Our previous work has shown that diabetogenic CD8 T cells in the islets of the non-obese diabetic (NOD) mouse model of T1D are phenotypically heterogenous, but CD8 T cell clonal heterogeneity in this model remains relatively unexplored. Here, we use paired single-cell RNA sequencing (scRNA-seq) and single-cell T cell receptor sequencing (scTCR-seq) to characterize autoreactive CD8 T cells from the islets and spleens of NOD mice. Clonal analysis of scTCR-seq data demonstrates that CD8 T cells targeting the immunodominant β cell epitope IGRP206-214 exhibit highly restricted TCR gene usage, with over 70% of IGRP206-214-reactive cells utilizing the same TCR V alpha, J alpha, and V beta genes. Despite this, we observe only 5% overlap of IGRP206-214-reactive CD8 T cell clones between two groups of 10 NOD mice, demonstrating the immense TCR heterogeneity generated by junctional diversity during V(D)J recombination. scRNA-seq identifies two new clusters of autoreactive CD8 T cells in the islets and six clusters of diabetogenic CD8 T cells in the spleen, including multiple memory-like clusters and a population of exhausted cells. Strong clonal overlap between IGRP206-214-reactive CD8 T cells in the islets and spleen suggests that these cells may exit the islets and enter the peripheral circulation. Finally, we identify correlations between TCR J beta gene usage, which is less restricted than that of other TCR genes, and CD8 T cell clonal expansion as well as effector fate. Collectively, our work demonstrates that IGRP206-214-specific CD8 T cells are phenotypically heterogeneous but clonally similar, raising the possibility of selectively targeting either conserved or divergent TCR structures of these cells for therapeutic benefit.

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