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Arid5a directs autoimmune inflammation through an IL-17 signaling pathway [human]

ABSTRACT: Arid5a directs autoimmune inflammation through an IL-17 signaling pathway [human]

PROVIDER: PRJNA1123383 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29383500_1.fastq.gz	Fastqsanger.gz
	SRR29383500_2.fastq.gz	Fastqsanger.gz
	SRR29383501_1.fastq.gz	Fastqsanger.gz
	SRR29383501_2.fastq.gz	Fastqsanger.gz
	SRR29383502_1.fastq.gz	Fastqsanger.gz

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Arid5a directs autoimmune inflammation through an IL-17 signaling pathway [mouse]

Project description:Arid5a directs autoimmune inflammation through an IL-17 signaling pathway [mouse]

| PRJNA1123382 | ENA

Arid5a directs autoimmune inflammation through an IL-17 signaling pathway [mouse]

Project description:Using Arid5a deficient mice to study the role of the RNA-binding protein Arid5a in models of autoimmunity, namely autoimmune glomerulonephritis

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Arid5a directs autoimmune inflammation through an IL-17 signaling pathway [human]

Project description:Using Arid5a deficient mice to study the role of the RNA-binding protein Arid5a in models of autoimmunity, namely autoimmune glomerulonephritis

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CMTM4 is a subunit of the IL-17 receptor and mediates autoimmune pathology

Project description:Interleukin-17A (IL-17A) is a key mediator of protective immunity to yeast and bacterial infections but also drives the pathogenesis of several autoimmune diseases, such as psoriasis or psoriatic arthritis. Here, we show that the tetra-transmembrane protein CMTM4 is a subunit of the IL-17 receptor (IL-17R). CMTM4 constitutively associated with IL-17R subunit C (IL-17RC) to mediate its stability, posttranslational modification, and plasma membrane localization. Both mouse and human cell lines deficient in CMTM4 were largely unresponsive to IL-17A, due to their inability to assemble the IL-17 receptor signaling complex. Accordingly, CMTM4-deficient mice were largely resistant to experimental psoriasis. Collectively, our data identified CMTM4 as an essential component of the IL-17 receptor and a potential therapeutic target for treating IL-17-mediated autoimmune diseases.

2022-12-02 | PXD036366 | Pride

Insights into the role of de novo fatty acid synthesis in IL-17-producing γδ T cells upon psoriatic inflammation

Project description:γδ T cells produce the primary innate source of IL-17 (γδT17) and are known to play a critical role in autoimmune and inflammatory diseases such as psoriasis. We here reported that psoriatic condition (IL-1b and IL-23) reshaped metabolic signatures and effector function of γδT17 cells compared to homeostatic condition (IL-7). Acetyl-CoA carboxylase 1 (ACC1), a rate-limiting enzyme of fatty acid synthesis (FAS), directs the fate of IL-17-producing CD4 T cells (Th17) differentiation. However, little is known about the role of ACC1-mediated FAS in their innate IL-17-producer counterpart, γδT17 cells. We further investigated the role of FAS in γδT17 by comparing the effect of pharmacological ACC inhibitor Soraphen A (SorA) on DMSO vehicle under psoriatic conditions (IL-1b and IL-23) to provide insights for clinical implication.

2025-02-20 | PXD050505 | JPOST Repository

The m6A reader IMP2 directs autoimmune inflammation through an IL-17- and TNFa-dependent C/EBP transcription factor axis

Project description:The m6A reader IMP2 directs autoimmune inflammation through an IL-17- and TNFa-dependent C/EBP transcription factor axis

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The m6A reader IMP2 directs autoimmune inflammation through an IL-17– and TNFa-dependent C/EBP transcription factor axis

Project description:The m6A reader IMP2 directs autoimmune inflammation through an IL-17– and TNFa-dependent C/EBP transcription factor axis

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Systematic analysis of IL-17 receptor signalosome reveals a robust regulatory feedback loop

Project description:IL-17 mediates immune protection from fungi and bacteria as well as it promotes autoimmune pathologies. However, the regulation of the signal transduction from the IL-17 receptor (IL-17R) remained elusive. We developed a novel mass spectrometry-based approach to identify components of the IL-17R complex followed by analysis of their roles using reverse genetics. Besides the identification of LUBAC as an important signal transducing component of IL-17R, we established that IL-17 signaling is regulated by a robust negative feedback loop mediated by TBK1 and IKKε. These kinases terminate IL-17 signaling by phosphorylating the adaptor ACT1 leading to the release of the essential ubiquitin ligase TRAF6 from the complex. NEMO recruits both kinases to the IL-17R complex, documenting that NEMO has an unprecedented negative function in IL-17 signaling, distinct from its role in NF-κB activation. Our study provides a comprehensive view of the molecular events of the IL-17 signal transduction and its regulation.

2020-07-15 | PXD019020 | Pride

Effect of fatty acid synthesis inhibition in IL-17-producing gamma delta T (γδT17) cells upon psoriatic inflammation

Project description:γδ T cells represent the primary innate source of IL-17 (γδT17) and are known to play a critical role in autoimmune and inflammatory diseases such as psoriasis. We here reported that psoriatic condition (IL-1b and IL-23) reshaped γδT17 cell metabolic signatures and promoted cytokine expression levels compared to homeostatic condition (IL-7). Acetyl-CoA carboxylase 1 (ACC1), a rate-limiting enzyme of fatty acid synthesis (FAS), directs the fate of IL-17-producing CD4 T cells (Th17) differentiation. However, little is known about the role of ACC1-mediated FAS in their innate IL-17-producer counterpart, γδT17 cells. We further investigated the role of FAS in γδT17 by comparing the effect of pharmacological inhibitor Soraphen A (SorA) on DMSO vehicle under psoriatic conditions (IL-1b and IL-23). Interestingly, ACC inhibition shifts the lipid metabolism in γδT17 cells, which allows them to cope with lipid demand without affecting cellular viability.

2025-02-20 | GSE256512 | GEO

IL-17-induced NF-kB activation via CIKS/Act1: Physiologic significance and signaling mechanisms

Project description:Interleukin-17 (IL-17) is essential in host defense against extracellular bacteria and fungi, especially at mucosal sites, but it also contributes significantly to inflammatory and autoimmune disease pathologies. Binding of IL-17 to its receptor leads to recruitment of the adaptor protein CIKS/Act1 via heterotypic association of their respective SEFIR domains and to activation of the transcription factor NF-kB; it is not known whether CIKS and/or NF-kB are required for all gene induction events. Here we report that CIKS is essential for all IL-17 induced immediate-early genes in primary mouse embryo fibroblasts, while NF-kB is profoundly involved. We also identify a novel sub-domain in the N-terminus of CIKS that is essential for IL-17-mediated NF-kB activation. This domain is both necessary and sufficient for the interaction between CIKS and TRAF6, an adaptor required for NF-kB activation. The ability of decoy peptides to block this interaction may provide a new therapeutic strategy for intervention in IL-17-driven autoimmune and inflammatory diseases. Keywords: strain comparisons strain comparisons

2011-10-18 | E-GEOD-24873 | biostudies-arrayexpress

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