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Effect of LINC01871 silencing on CD4+ T cell activation.

ABSTRACT: Effect of LINC01871 silencing on CD4+ T cell activation.

PROVIDER: PRJNA1117406 | ENA |

REPOSITORIES: ENA

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Effect of LINC01871 silencing on CD4+ T cell activation.

Project description:Long intergenic noncoding RNAs (lincRNAs) play crucial roles in regulating biological processes in health and disease. However, little is known about the contribution of lincRNAs in T-cell activation. Here, we identified a lincRNA, LINC01871, which is highly induced upon T-cell activation and is predominantly located in the cytoplasm. The anti-inflammatory cytokine TGF-β was found to suppress its expression. Silencing LINC01871 led to a modest decrease in IL-2 secretion. RNA-seq and proteomic analyses of LINC01871-deficient CD4+ T cells revealed several targets, including genes associated with autophagy and membrane organization such as ATG2B; TRIM5; SNX30; TIMM8B; and ATP10A. Notably, LINC01871 expression was highly specific to T cells in several cross tissue single cell RNA-seq atlases. Furthermore, ex-vivo CD4+ T cells from children progressing to beta-cell autoimmunity showed higher LINC01871 expression as compared to their age, sex and HLA-risk matched controls. These data suggest that LINC01871 has an in-vivo function in T-cell-mediated immunity.

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A metabolism-epigenome axis controls early events in CD4+ T cell activation

Project description:Upon antigen-specific T Cell Receptor (TCR) engagement, human CD4+ T cells proliferate and differentiate, a process associated with rapid transcriptional changes and metabolic reprogramming utilizing aerobic glycolysis together with maintenance of oxidative phosphorylation1,2. However, the role of glycolytic-reprogramming during T-cell activation remains largely unclear3,4,5. Here, we show that maintenance of cytosolic pyruvate production is an essential requirement for remodeling of the CD4+ T cell epigenome after TCR-engagement. Furthermore, we provide evidence that the local inflammatory environment sustains metabolic reprogramming of CD4+ T-cells and impacts histone modification in a pyruvate-dependent manner. Mechanistically, we demonstrate that rapid and sustained generation of cytosolic, but not mitochondrial, pyruvate is an essential step for acetyl-coA production and subsequent H3K27ac epigenome remodeling. TCR-activation was found to induce nuclear import of pyruvate dehydrogenase (PDH) and its association with both the p300 acetyltransferase and histone H3K27ac. Disrupting PDH nuclear import impacted expression of activation-induced genes. These results reveal a direct connection between CD4+ T cell metabolic reprogramming and transcriptional regulation, with the generation of cytosolic pyruvate being an essential step in T cell activation. These data support tight integration of metabolic enzymes and histone modifying enzymes, allowing metabolic reprogramming to fuel CD4+ T cell activation.

2023-10-27 | PXD018132 | Pride

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