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PPARg Deficiency Suppresses the Release of IL-1b and a in Macrophages via a Type 1 Interferon Dependent Mechanism

ABSTRACT: PPARg Deficiency Suppresses the Release of IL-1b and a in Macrophages via a Type 1 Interferon Dependent Mechanism

PROVIDER: PRJNA481067 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7521790.fastq.gz	Fastqsanger.gz
	SRR7521800.fastq.gz	Fastqsanger.gz
	SRR7521791.fastq.gz	Fastqsanger.gz
	SRR7521801.fastq.gz	Fastqsanger.gz
	SRR7521792.fastq.gz	Fastqsanger.gz

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Type I Interferon promotes MxA-dependent IL-1b release in SLE monocytes

Project description:Systemic lupus erythematosus (SLE) is characterized by upregulation of Type Ι Interferon (IFN) and widespread inflammation. However, blocking the IFN pathway benefits a fraction of patients, pointing to additional pathogenic players. Here we describe monocytes (Mo) undergoing erythrophagocytosis and co-expressing IFN-inducible genes (ISGs) and interleukin-1b (IL-1b) in patients with active disease. This phenotype is recapitulated in vitro upon internalization of red blood cells carrying mitochondria (Mito+ RBCs), a feature of SLE. While ISG expression requires the interaction between Mito+ RBC-derived mitochondrial DNA (mtDNA) and cGAS, the production of IL-1b entails Mito+ RBC-derived mitochondrial RNA (mtRNA) triggering RIG-I-like receptor (RLR) activation. This leads to the cytosolic release of Mo-derived mtDNA and activation of the NLRP3 inflammasome. Importantly, the Type I IFN-inducible protein myxovirus resistant protein 1 (MxA) enables IL-1b release by routing this cytokine into a trans-Golgi network (TGN)-mediated unconventional secretory pathway. As Type I IFN and IL-1b are thought to counter-regulate each other, our study highlights an unprecedented synergy between these two cytokine pathways in SLE.

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Project description:Inflammation is critical for controlling infections but can cause disease when unchecked. For tuberculosis, the leading cause of death by infection, neutrophil-dominated inflammation is associated with disease progression, emphasizing the need to understand how neutrophil functions are regulated during Mycobacterium tuberculosis infection. Atg5 was the first gene shown to specifically function within neutrophils to promote control of M. tuberculosis. ATG5 is best studied for its role in autophagy, however, the protective activity of ATG5 in neutrophils was unexpectedly independent of other autophagy proteins and remained elusive. We report that ATG5 is required in neutrophils to suppress type I interferon-induced neutrophil extracellular trap (NET) release and swarming during M. tuberculosis infection. Elevated NET release contributes to the early susceptibility of Atg5fl/fl-LysM-Cre mice during infection. These findings identify ATG5 as a master regulator of how type I interferon influences neutrophil responses during infection, revealing a new potential target for host-directed therapies.

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PPARg Deficiency Suppresses the Release of IL-1b and a in Macrophages via a Type 1 Interferon Dependent Mechanism

Project description:TG elicited Peritoneal macrophages from WT and PPARgamma KO mice were treated with control or lipid inflammatory stress in triplicate

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Cell line stimulated with recombinant cytokines interleukin-1b and interferon gamma.

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