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Effector Memory T cells induce DC-intrinsic DNA damage and a non-canonical STING pathway during innate inflammation

ABSTRACT: Effector Memory T cells induce DC-intrinsic DNA damage and a non-canonical STING pathway during innate inflammation

PROVIDER: PRJNA950996 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24037327_1.fastq.gz	Fastqsanger.gz
	SRR24037327_2.fastq.gz	Fastqsanger.gz
	SRR24037328_1.fastq.gz	Fastqsanger.gz
	SRR24037328_2.fastq.gz	Fastqsanger.gz
	SRR24037329_1.fastq.gz	Fastqsanger.gz

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Effector Memory T cells induce DC-intrinsic DNA damage and a non-canonical STING pathway during innate inflammation

Project description:A breach in tolerance to self-antigens induces expansion of autoreactive T cells, ultimately leading to autoimmune inflammation. While autoreactive T cells are principal drivers of autoimmunity, tissue pathology is alternatively driven by innate cytokines, indicating that autoreactive T cells can induce innate inflammation. This study has led to the discovery that effector memory T (Tem) cells trigger double stranded breaks via mitochondrial ROS production in interacting DCs. Consequently, initiation of the DNA damage response leads to activation of a cGAS-independent, STING-TRAF6-NFkB signaling axis. STING deficient DCs display significant defects in transcriptional induction and functional production of IL-1b and IL-6 following their interaction with Tem cells, both in vitro and in vivo. The discovery of Tem induced innate inflammation through DNA damage and a non-canonical STING-mediated NFkB activation presents this pathway as a potential target to alleviate T cell driven autoimmune inflammation.

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Effector Memory T cells induce DC-intrinsic DNA damage and a non-canonical STING pathway during innate inflammation [ATAC]

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Project description:Inflammatory diseases such as Aicardi-Goutieres Syndrome (AGS) and severe systemic lupus erythematosus (SLE) are generally lethal disorders that have been traced to defects in the exonuclease Trex1 (DNAseIII). Mice lacking Trex1 similarly die at an early age through comparable symptoms, including inflammatory myocarditis, through chronic activation of the STING (stimulator of interferon genes) pathway. Here we demonstrate that phagocytes rather than myocytes are predominantly responsible for causing inflammation, an outcome that could be alleviated following adoptive transfer of normal bone marrow into Trex1-/- mice. Trex1-/- macrophages did not exhibit significant augmented ability to produce pro-inflammatory cytokines compared to normal macrophages following exposure to STING-dependent activators, but rather appeared chronically stimulated by genomic DNA. These results shed molecular insight into inflammation and provide concepts for the design of new therapies. Total RNA obtained from wild type (WT), Trex1 deficient (TKO), STING deficient (SKO), or Trex1 and STING double deficient (STKO) mouse Heart

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