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Neutrophil extracellular trap induced dendritic cell activation leads to Th1 polarization in type 1 diabetes

ABSTRACT: Neutrophil extracellular trap induced dendritic cell activation leads to Th1 polarization in type 1 diabetes

PROVIDER: PRJNA599088 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10829901.fastq.gz	Fastqsanger.gz
	SRR10829902.fastq.gz	Fastqsanger.gz
	SRR10829903.fastq.gz	Fastqsanger.gz
	SRR10829904.fastq.gz	Fastqsanger.gz
	SRR10829905.fastq.gz	Fastqsanger.gz

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Neutrophil extracellular trap induced dendritic cell activation leads to Th1 polarization in type 1 diabetes

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Neutrophil Extracellular Trap Induced Dendritic Cell Activation Leads to Th1 Polarization in Type 1 Diabetes.

Project description:Neutrophils releasing neutrophil extracellular traps (NETs) infiltrate the pancreas prior to type 1 diabetes (T1D) onset; however, the precise nature of their contribution to disease remains poorly defined. To examine how NETs affect immune functions in T1D, we investigated NET composition and their effect on dendritic cells (DCs) and T lymphocytes in T1D children. We showed that T1D patient NET composition differs substantially from that of healthy donors and that the presence of T1D-NETs in a mixed peripheral blood mononuclear cell culture caused a strong shift toward IFN?-producing T lymphocytes, mediated through activation of innate immunity cells in T1D samples. Importantly, in a monocyte-derived DC (moDC) culture, NETs induced cytokine production, phenotypic change and IFN?-producing T cells only in samples from T1D patients but not in those from healthy donors. RNA-seq analysis revealed that T1D-NETs presence causes TGF? downregulation and IFN? upregulation and creates pro-T1D signature in healthy moDCs.

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NFE2-driven neutrophil polarization promotes pancreatic cancer liver metastasis progression

Project description:Pancreatic cancer liver metastasis (PCLM) is an important factor leading to dismal prognosis. The adaptive remodeling of the tumor microenvironment (TME), especially the role of neutrophil in liver metastasis remains elusive. Here we combined single-cell sequencing combined with spatial transcriptomics on patients’ samples to characterize the landscape of PCLM, and explored the functional diversity possessed by neutrophils infiltrated in liver metastases. We identified the pivotal Neutrophils_S100A12 cluster capable of promoting metastatic progression by releasing neutrophil extracellular traps (NETs); spatially, Neutrophils_S100A12 cells are specifically distributed at the invasive front of the metastatic lesions. Mechanistically metastatic TME activates canonical TGF-β/SMAD3 signaling within neutrophil, resulting in NFE2-mediated phenotypic polarization; furthermore NFE2 induces NETs generation by up-regulating PADI4 expression. Interference with NFE2 activation in neutrophils prevents phenotypic conversion and reduces liver metastasis. Our data demonstrate that NFE2-mediated neutrophil polarization in PCLM is a potential target for anti-metastatic therapy.

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P2X7 signaling drives Th1 cell differentiation through metabolic reprogramming for aerobic glycolysis

Project description:This study provides evidence on the molecular mechanisms by which P2RX7 signaling promotes Th1 cell differentiation. P2RX7 induces T-bet expression and aerobic glycolysis in splenic CD4+ T cells that respond to malaria, at a time prior to Th1/Tfh polarization. Cell-intrinsic P2RX7 signaling sustains the glycolytic pathway and causes bioenergetic mitochondrial stress in activated CD4+ T cells. We also show in vitro the phenotypic similarities of Th1-polarized CD4+ T cells that do not express P2RX7 and those in which the glycolytic pathway is pharmacologically inhibited. In addition, ATP synthase blockade in vitro and the consequent inhibition of oxidative phosphorylation, which forces cells to use aerobic glycolysis, is sufficient to promote rapid CD4+ T cell proliferation and polarization to the Th1 profile in the absence of P2RX7. These data demonstrate that P2RX7-mediated metabolic reprograming for aerobic glycolysis is a key event for Th1 cell differentiation and suggest that ATP synthase inhibition is a fundamental mechanism by which P2X7 signaling induces the Th1 response.

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