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Long non-coding RNA LINC01882 ameliorates aGVHD via skewing CD4+ T Cells differentiation towards Treg cells

ABSTRACT: Long non-coding RNA LINC01882 ameliorates aGVHD via skewing CD4+ T Cells differentiation towards Treg cells

PROVIDER: PRJNA878706 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21497252_1.fastq.gz	Fastqsanger.gz
	SRR21497252_2.fastq.gz	Fastqsanger.gz
	SRR21497253_1.fastq.gz	Fastqsanger.gz
	SRR21497253_2.fastq.gz	Fastqsanger.gz

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Long non-coding RNA LINC01882 ameliorates aGVHD via skewing CD4+ T Cells differentiation towards Treg cells

Project description:To investigate the function of long non-coding RNA LINC01882 in the regulation of CD4+T cell differentiation, we established LINC01882-overexpressed CD4+T cells by infecting with lentivirus. We then performed microRNA gene expression profiling analysis using data obtained from microRNA sequencing.

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Transcriptional profiling of PBMC from patients with aGvHD and patients without aGvHD after alloHSCT

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Project description:Human FOXP3+ regulatory T (Treg) cells are central to immune tolerance. However, their heterogeneity and differentiation remain incompletely understood. Here we use single-cell RNA and T cell receptor sequencing to resolve Treg cells from healthy individuals and patients with or without acute graft-versus-host disease (aGVHD) who undergo stem cell transplantation. These analyses, combined with functional assays, separate Treg cells into naïve/activated/effector stages, and resolve the HLA-DRhi, LIMS1hi, highly suppressive FOXP3hi, and highly proliferative MKI67hi effector subsets. Trajectory analysis assembles Treg subsets into two differentiation paths (I/II) with distinctive phenotypic/functional programs, ending with the FOXP3hi and MKI67hi subsets, respectively. Transcription factors FOXP3 and SUB1 contribute to some Path I and Path II phenotypes, respectively. These FOXP3hi and MKI67hi subsets and two differentiation pathways are conserved in transplanted patients, despite having functional/migratory impairments under aGVHD. The findings expand the understanding of Treg cell heterogeneity and differentiation and provide a single-cell atlas for the dissection of Treg complexity in health and disease.

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