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Tissue-resident PSGL1loCD4+ T cells promote B cell differentiation and chronic graft-versus-host-disease-associated autoimmunity

ABSTRACT: Tissue-resident PSGL1loCD4+ T cells promote B cell differentiation and chronic graft-versus-host-disease-associated autoimmunity

PROVIDER: PRJNA661763 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12601007.fastq.gz	Fastqsanger.gz
	SRR12601008.fastq.gz	Fastqsanger.gz
	SRR12601009.fastq.gz	Fastqsanger.gz
	SRR12601010.fastq.gz	Fastqsanger.gz
	SRR12601011.fastq.gz	Fastqsanger.gz

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Tissue-resident PSGL1loCD4+ T cells promote B cell differentiation and chronic graft-versus-host disease-associated autoimmunity.

Project description:CD4+ T cell interactions with B cells play a critical role in the pathogenesis of systemic autoimmune diseases such as systemic lupus and chronic graft-versus-host disease (cGVHD). Extrafollicular CD44hiCD62LloPSGL1loCD4+ T cells (PSGL1loCD4+ T cells) are associated with the pathogenesis of lupus and cGVHD, but their causal role has not been established. With murine and humanized MHC-/-HLA-A2+DR4+ murine models of cGVHD, we showed that murine and human PSGL1loCD4+ T cells from GVHD target tissues have features of B cell helpers with upregulated expression of programmed cell death protein 1 (PD1) and inducible T cell costimulator (ICOS) and production of IL-21. They reside in nonlymphoid tissues without circulating in the blood and have features of tissue-resident memory T cells with upregulated expression of CD69. Murine PSGL1loCD4+ T cells from GVHD target tissues augmented B cell differentiation into plasma cells and production of autoantibodies via their PD1 interaction with PD-L2 on B cells. Human PSGL1loCD4+ T cells were apposed with memory B cells in the liver tissues of humanized mice and cGVHD patients. Human PSGL1loCD4+ T cells from humanized GVHD target tissues also augmented autologous memory B cell differentiation into plasma cells and antibody production in a PD1/PD-L2-dependent manner. Further preclinical studies targeting tissue-resident T cells to treat antibody-mediated features of autoimmune diseases are warranted.

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Project description:RATIONALE: Beclomethasone may be an effective treatment for graft-versus-host disease. PURPOSE: Phase I/II trial to study the effectiveness of beclomethasone in treating patients who have graft-versus-host disease of the esophagus, stomach, small intestine, or colon.

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6-phosphogluconate dehydrogenase blockade in T Cells mitigates acute graft-versus-host disease while preserving graft-versus-tumor activity

Project description:6-phosphogluconate dehydrogenase blockade in T Cells mitigates acute graft-versus-host disease while preserving graft-versus-tumor activity

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Tissue-resident PSGL1loCD4+ T cells promote B cell differentiation and chronic graft-versus-host-disease-associated autoimmunity

Project description:We report application of RNA-seqencing to investigate PSGL1hi and PSGL1lo CD4+T cells transcriptional difference in the GVHD target tissues of spleen, liver and lung at day 30 after HCT.

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6-phosphogluconate dehydrogenase blockade in T Cells mitigates acute graft-versus-host disease while preserving graft-versus-tumor activity

Project description:T cells undergo significant metabolic reprogramming after allogeneic hematopoietic cell transplantation (allo-HCT). However, the influence of metabolic pathway reprogramming on altering the severity and mortality of acute graft-versus-host disease (aGvHD), a critical allo-HCT complication, remains unclear. Through single-cell RNA sequencing (scRNA-seq) of allogeneic T cells isolated from the spleen of GvHD mice, we uncovered that 6-phosphogluconate dehydrogenase (6PGD), the second major rate-limiting enzyme in the oxidative pentose phosphate pathway, is upregulated and activated during allo-HCT. Clinical and histopathological analyses revealed that 6PGD deficiency in donor T cells significantly mitigates aGvHD severity and mortality in murine models of acute GvHD. An in vitro assay using murine and human T cells and an in vivo murine GvHD model showed that in the absence of an intact 6PGD pathway, donor T cell proliferation was reduced. Metabolic analyses confirmed that blocking 6PGD activity shifted T cell metabolism from glycolysis to oxidative phosphorylation (OXPHOS), as evidenced by isotope-labeled metabolic tracing and Seahorse assays. Pharmacological inhibition of 6PGD with 6-aminonicotinamide (6AN) demonstrated similar efficacy as the infusion of donor 6PGD deficient T cells in reducing aGvHD severity in allogeneic aGvHD and humanized xenogeneic GvHD models. Importantly, 6PGD inhibition preserved the graft-versus-tumor (GvT) effect by promoting the generation of a small subset of effector T cells with potent anti-tumor activity. From these findings we propose 6PGD as a promising therapeutic target for alleviating aGVHD the beneficial GvT effects.

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Project description:Allogeneic hematopoietic stem cell transplantation (HSCT) is the treatment of choice for high-risk hematological malignancies, yet a major complication associated with this therapy is acute graft-versus-host disease (GVHD). Despite a well-defined pathophysiological mechanism, there are no definitive markers for predicting acute GVHD development or progression to advanced stages. In the current study, we enrolled four acute GVHD and four acute GVHD-free recipients of allogeneic HSCT and collected peripheral blood just prior to onset of clinical acute GVHD for analysis on Affymetrix GeneChip Human Genome U133 Plus 2.0 microarrays. We noted significant differences in expression of 1,658 genes between control and acute GVHD patients, based on an analysis of covariance (ANCOVA) by type of transplant, a pooled error estimate, and a false discovery rate (FDR) of 10%. In conclusion, we offer the first report of a preliminary molecular signature of acute GVHD in allogeneic HSCT patients.

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