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Characterization and effective expansion of CD4-CD8- TCRab+ T cells from individuals living with type 1 diabetes

ABSTRACT: Characterization and effective expansion of CD4-CD8- TCRab+ T cells from individuals living with type 1 diabetes

PROVIDER: PRJNA1204964 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31864456.fastq.gz	Fastqsanger.gz
	SRR31864457.fastq.gz	Fastqsanger.gz
	SRR31864458.fastq.gz	Fastqsanger.gz
	SRR31864459.fastq.gz	Fastqsanger.gz
	SRR31864460.fastq.gz	Fastqsanger.gz

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Characterization and effective expansion of CD4-CD8- TCRab+ T cells from individuals living with type 1 diabetes

Project description:CD4-CD8- TCRab+ (double-negative [DN]) T cells represent a rare T cell population that promotes immunological tolerance through various cytotoxic mechanisms. In mice, autologous transfer of DN T cells has shown protective effects against autoimmune diabetes and graft-versus-host disease. Here, we characterized humanDNT cells from people living with type 1 diabetes (PWT1D) and healthy controls. We found that while DN T cells and CD8+ T cells share many similarities, DN T cells are a unique T cell population, both at the transcriptomic and protein levels. We also show that by using various cytokine combinations, human DN T cells can be expanded in vitro up to 1,000- fold (mean >250-fold) and remain functional post-expansion. In addition, we report that DN T cells from PWT1D display a phenotype comparable to that of healthy controls, efficiently expand, and are highly functional. As DN T cells are immunoregulatory and can prevent T1D in various mouse models, these observations suggest that autologous DN T cells may be amenable to therapy for the prevention or treatment of T1D.

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2021-02-26 | E-MTAB-8891 | biostudies-arrayexpress

Genetic code expansion reveals site-specific lactylation in living cells reshapes protein function

Project description:Still in its infancy, the functions of lactylation remain elusive. To address this, we established a comprehensive workflow for lactylation studies that integrates the discovery of lactylation sites with proteomics, the expression of site-specifically lactylated proteins in living cells via genetic code expansion (GCE), and the evaluation of the resulting biological consequences. Specifically, we developed a wet-and-dry-lab combined proteomics strategy, and identified highly conserved lactylation at ALDOA-K147. Driven by its potential biological significance, we site-specifically expressed this lactylated ALDOA in mammalian cells and interrogated the biological changes. We discovered that it not only inhibited enzyme activity but also elicited gain-of-function effects——it dramatically reshaped the functionality of ALDOA by improving stability, enhancing nuclear translocation and affecting gene expression. Further, we demonstrated broad applicability of this workflow to study distinct histone lactylation sites. Together, we anticipate its wide uses in elucidating causative links between site-specific lactylation and target-centric or cell-wide changes.

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Project description:Naive CD4 T cells defined as (TCRab+ CD4+ CD45RA+ CD62L+ CD127+) were further divided by CD25 and CD31 expression with FACS-based flow sorting. Subsequently, gene expression levels of each subset were assessed by using transcription arrays.

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Pharmacological activation of LRH-1/NR5A2 triggers an anti-inflammatory phenotypic switch in immune cells from individuals with type 1 diabetes and improves human islet engraftment/function

Project description:The intricate aetiology of type 1 diabetes mellitus (T1DM) implicating a detrimental cross talk between immune cells and insulin producing b-cells leading to their destruction has stumped the development of effective disease modifying therapies. The discovery that the pharmacological activation of LRH-1/NR5A2 can revert hyperglycemia in pre-clinical mouse models of T1DM by attenuating the autoimmune attack coupled to b-cell survival/regeneration, prompt us to investigate whether LRH-1/NR5A2-mediated immune tolerization could be achieved in individuals with T1DM and improve islet survival and function subsequent to xenotransplantation. We found that LRH-1/NR5A2 activation using the agonist BL001 blunted the pro-inflammatory genetic signature and cytokine secretome of both monocyte-derived macrophages (MDM1) and mature dendritic cells (mDCs) from individuals with T1DM. Mechanistically, mitohormesis was induced in MDM1 restricting pro-inflammation propagation while mitochondria turnover was increased in mDCs assisting transit towards a tolerogenic phenotype. BL001 treatment also increased T-regulatory cells within the T-cell subpopulation. BL001-treated MDM1, mDCs or T-cells impeded T-effector cell expansion. Engraftment and function of human islets transplanted into hyperglycemic immunocompetent mice was enhanced by BL001 treatment leading to improved glycemia. Collectively, LRH-1/NR5A2 agonism fosters a coordinated re-programming of T1DM immune cells from a pro- to an anti-inflammatory/tolerizing phenotype empowering them to repress cytotoxic T-cell proliferation and facilitates islet engraftment and function after transplantation. Our finding demonstrate the feasibility of re-establishing human immune tolerance within a pro-inflammatory environment, rather than suppression, opening an unprecedent pharmacological therapeutic venue for T1DM

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Pharmacological activation of LRH-1/NR5A2 triggers an anti-inflammatory phenotypic switch in immune cells from individuals with type 1 diabetes and improves human islet engraftment/function

Project description:The intricate aetiology of type 1 diabetes mellitus (T1DM) implicating a detrimental cross talk between immune cells and insulin producing -cells leading to their destruction has stumped the development of effective disease modifying therapies. The discovery that the pharmacological activation of LRH-1/NR5A2 can revert hyperglycemia in pre-clinical mouse models of T1DM by attenuating the autoimmune attack coupled to -cell survival/regeneration, prompt us to investigate whether LRH-1/NR5A2-mediated immune tolerization could be achieved in individuals with T1DM and improve islet survival and function subsequent to xenotransplantation. We found that LRH-1/NR5A2 activation using the agonist BL001 blunted the pro-inflammatory genetic signature and cytokine secretome of both monocyte-derived macrophages (MDM1) and mature dendritic cells (mDCs) from individuals with T1DM. Mechanistically, mitohormesis was induced in MDM1 restricting pro-inflammation propagation while mitochondria turnover was increased in mDCs assisting transit towards a tolerogenic phenotype. BL001 treatment also increased T-regulatory cells within the T-cell subpopulation. BL001-treated MDM1, mDCs or T-cells impeded T-effector cell expansion. Engraftment and function of human islets transplanted into hyperglycemic immunocompetent mice was enhanced by BL001 treatment leading to improved glycemia. Collectively, LRH-1/NR5A2 agonism fosters a coordinated re-programming of T1DM immune cells from a pro- to an anti-inflammatory/tolerizing phenotype empowering them to repress cytotoxic T-cell proliferation and facilitates islet engraftment and function after transplantation. Our finding demonstrate the feasibility of re-establishing human immune tolerance within a pro-inflammatory environment, rather than suppression, opening an unprecedent pharmacological therapeutic venue for T1DM.

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