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Interleukin-2 receptor signaling acts as a checkpoint that shapes the distribution of regulatory T cell subsets (RNA-Seq)

ABSTRACT: Interleukin-2 receptor signaling acts as a checkpoint that shapes the distribution of regulatory T cell subsets (RNA-Seq)

PROVIDER: PRJNA1114062 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29103865_1.fastq.gz	Fastqsanger.gz
	SRR29103865_2.fastq.gz	Fastqsanger.gz
	SRR29103866_1.fastq.gz	Fastqsanger.gz
	SRR29103866_2.fastq.gz	Fastqsanger.gz
	SRR29103867_1.fastq.gz	Fastqsanger.gz

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Interleukin-2 receptor signaling acts as a checkpoint that shapes the distribution of regulatory T cell subsets

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Interleukin-2 receptor signaling acts as a checkpoint that shapes the distribution of regulatory T cell subsets (scRNA-Seq)

Project description:Regulatory T cells (Tregs) require IL-2 for survival in the periphery, yet how IL-2 shapes Treg heterogeneity remains poorly defined. Here we found that inhibition of IL-2R signaling in post-thymic Tregs leads to a preferential early loss of central Tregs (cTregs). Gene expression of cTregs was more dependent on IL-2R signaling than effector Tregs (eTregs). Unexpectedly, ablation of IL-2R signaling in cTregs resulted in increased proliferation, expression of eTreg genes, and enhanced capacity to develop into eTregs. These findings indicate that physiological amounts of IL-2 act as a checkpoint to maintain cTreg homeostasis and tolerance while restraining their development into eTregs. Nevertheless, direct evaluation of eTregs revealed that loss of IL-2R signaling alters the distribution of eTreg subsets, with increased IFNgR1+ eTregs and CXCR5+ PD-1+ T follicular regulatory (TFR) cells but decreased intestinal RORgt+ TR17 cells. Thus, IL-2R signaling also shapes the development of specialized eTregs subsets.

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Interleukin-2 receptor signaling acts as a checkpoint that shapes the distribution of regulatory T cell subsets (RNA-Seq)

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Extracellular Lactate Acts as a Metabolic Checkpoint and Shapes Monocyte Function Time Dependently.

Project description:Elevated blood lactate levels are frequently found in critically ill patients and thought to result from tissue hypoperfusion and cellular oxygen shortage. Considering the close relationship between immune cell function and intracellular metabolism, lactate is more than a glycolytic waste molecule but able to regulate the immune response. Our aim was to elucidate the temporal and mechanistic effect of extracellular lactate on monocytes. To this end, primary human monocytes and the human monocytic cell line MonoMac6 were stimulated with various toll-like-receptor agonists after priming with Na-L-lactate under constant pH conditions. As readout, cytokine production was measured, real-time assessment of intracellular energy pathways was performed, and intracellular metabolite concentrations were determined. Irrespective of the immunogenic stimulus, short-term Na-lactate-priming strongly reduced cytokine production capacity. Lactate and hexoses accumulated intracellularly and, together with a decreased glycolytic flux, indicate a lactate-triggered impairment of glycolysis. To counteract intracellular hyperglycemia, glucose is shunted into the branching polyol pathway, leading to sorbitol accumulation. In contrast, long-term priming with Na-L-lactate induced cellular adaption and abolished the suppressive effect. This lactate tolerance is characterized by a decreased cellular respiration due to a reduced complex-I activity. Our results indicate that exogenous lactate shapes monocyte function by altering the intracellular energy metabolism and acts as a metabolic checkpoint of monocyte activation.

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