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ABSTRACT: Interspecies transcriptome profiles of human T cell activation and liver inflammation in a xenogeneic graft-versus-host disease model

PROVIDER: PRJNA1013270 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25921575_1.fastq.gz	Fastqsanger.gz
	SRR25921575_2.fastq.gz	Fastqsanger.gz
	SRR25921576_1.fastq.gz	Fastqsanger.gz
	SRR25921576_2.fastq.gz	Fastqsanger.gz
	SRR25921577_1.fastq.gz	Fastqsanger.gz

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Project description:Abundant donor cytotoxic T cells that attack normal host organs remain a major problem for patients receiving allogeneic hematopoietic cell transplantation (Allo-HCT). Despite an increase in our knowledge of the pathobiology of acute graft versus host disease (aGvHD), the mechanisms regulating the proliferation and function of donor T cells remain unclear. Here, we show that activated donor T cells express galectin-3 (Gal-3) after allo-HCT. In both major and minor histocompatibility–mismatched models of murine aGvHD, expression of Gal-3 is associated with decreased T cell activation and suppression of the secretion of effector cytokines including IFN-γ and GM-CSF. Mechanistically, Gal-3 results in activation of NFAT signaling which can induce T cell exhaustion. Gal-3 overexpression in human T cells prevents severe disease by suppressing cytotoxic T cells in xenogeneic aGvHD models. Together these data identify the Gal-3-dependent regulatory pathway in donor T cells as a critical component of inflammation in aGvHD.

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The effect of inhibition of arginine methylation in human FOXP3-transduced T cells

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