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STAT1 deficiency underlies a proinflammatory imprint of naive CD4+ T cells in spondyloarthritis [RNA-Seq]

ABSTRACT: STAT1 deficiency underlies a proinflammatory imprint of naive CD4+ T cells in spondyloarthritis [RNA-Seq]

PROVIDER: PRJNA1026891 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26349835_1.fastq.gz	Fastqsanger.gz
	SRR26349835_2.fastq.gz	Fastqsanger.gz
	SRR26349836_1.fastq.gz	Fastqsanger.gz
	SRR26349836_2.fastq.gz	Fastqsanger.gz
	SRR26349837_1.fastq.gz	Fastqsanger.gz

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STAT1 deficiency underlies a proinflammatory imprint of naive CD4+ T cells in spondyloarthritis

Project description:STAT1 deficiency underlies a proinflammatory imprint of naive CD4+ T cells in spondyloarthritis

| PRJNA1026882 | ENA

STAT1 deficiency underlies a proinflammatory imprint of naive CD4+ T cells in spondyloarthritis [RNA-Seq]

Project description:In spondyloarthritis (SpA), an increased type 3 immune response, including T helper cells (Th) 17 excess, is observed in both human and SpA animal models, such as the HLA-B27/human β2-microglobulin transgenic rat (B27-rat). To investigate this unexplained Th17-biased differentiation, we focused on understanding the immunobiology of B27-rat naive CD4+ T cells (Tn). We observed that neutrally stimulated B27-rat Tn developed heightened Th17 profile even before disease onset, suggesting an intrinsic proinflammatory predisposition. In parallel with this observation, transcriptomic and epigenomic analysis showed that B27-rat Tn exhibited a decreased expression of Interferon/Th1- and increased expression of Th17-related genes. This molecular signature was predicted to be related to an imbalance of STAT1/STAT3 transcription factors activity. Stat1 mRNA and STAT1 protein expression were decreased before disease onset in Tn, even in their thymic precursors, whereas Stat3/STAT3 expression increased upon disease establishment. Confirming the relevance of these results, STAT1 mRNA expression was also decreased in Tn from SpA patients, as compared with healthy controls and rheumatoid arthritis patients. Finally, stimulation of B27-rat Tn with a selective STAT1 activator abolished this preferential IL-17A expression, suggesting that STAT1 altered activity in B27-rats allows Th17 differentiation. Altogether, B27-rat Tn harbor a STAT1 deficiency preceding disease onset, that may occur during their thymic differentiation, secondarily associated with a persistent Th17 bias, which is imprinted at the epigenomic level. This early molecular phenomenon might lead to the persistent proinflammatory skew of CD4+ T cells in SpA patients, thus offering new clues to better understand and treat SpA.

2023-10-11 | GSE245066 | GEO

STAT1 deficiency underlies a proinflammatory imprint of naive CD4+ T cells in spondyloarthritis [ChIP-Seq]

2023-10-11 | GSE245064 | GEO

STAT1 deficiency underlies a proinflammatory imprint of naive CD4+ T cells in spondyloarthritis [ChIP-Seq]

Project description:STAT1 deficiency underlies a proinflammatory imprint of naive CD4+ T cells in spondyloarthritis [ChIP-Seq]

| PRJNA1026892 | ENA

STAT1 deficiency underlies a proinflammatory imprint of naive CD4<sup>+</sup> T cells in spondyloarthritis.

Project description:IntroductionIn spondyloarthritis (SpA), an increased type 3 immune response, including T helper cells (Th) 17 excess, is observed in both human and SpA animal models, such as the HLA-B27/human β2-microglobulin transgenic rat (B27-rat).MethodsTo investigate this unexplained Th17-biased differentiation, we focused on understanding the immunobiology of B27-rat naive CD4+ T cells (Tn).ResultsWe observed that neutrally stimulated B27-rat Tn developed heightened Th17 profile even before disease onset, suggesting an intrinsic proinflammatory predisposition. In parallel with this observation, transcriptomic and epigenomic analyses showed that B27-rat Tn exhibited a decreased expression of Interferon/Th1- and increased expression of Th17-related genes. This molecular signature was predicted to be related to an imbalance of STAT1/STAT3 transcription factors activity. Stat1 mRNA and STAT1 protein expression were decreased before disease onset in Tn, even in their thymic precursors, whereas Stat3/STAT3 expression increased upon disease establishment. Confirming the relevance of these results, STAT1 mRNA expression was also decreased in Tn from SpA patients, as compared with healthy controls and rheumatoid arthritis patients. Finally, stimulation of B27-rat Tn with a selective STAT1 activator abolished this preferential IL-17A expression, suggesting that STAT1-altered activity in B27-rats allows Th17 differentiation.DiscussionAltogether, B27-rat Tn harbor a STAT1 deficiency preceding disease onset, which may occur during their thymic differentiation, secondarily associated with a persistent Th17 bias, which is imprinted at the epigenomic level. This early molecular phenomenon might lead to the persistent proinflammatory skew of CD4+ T cells in SpA patients, thus offering new clues to better understand and treat SpA.

| S-EPMC10619905 | biostudies-literature

STAT1 deficiency underlies a proinflammatory imprint of naive CD4+ T cells in spondyloarthritis

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-10-11 | GSE245067 | GEO

Proteomics analysis of plasma from radiographic axial spondyloarthritis patients.

Project description:Tandem mass spectrometry analysis of proteins from depleted plasma from radiographic axial spondyloarthritis patients pre- and post-treated with adalimumab.

2024-05-02 | PXD026189 | Pride

Gene expression in juvenile spondyloarthritis

2014-10-31 | GSE58667 | GEO

Metagenomic Spondyloarthritis

Project description:Reciprocal inlfuence of TNF alpha inhibitor and microbiota composition in spondyloarthritis patients

| PRJEB19186 | ENA

Gene expression in juvenile spondyloarthritis

Project description:Association of juvenile spondyloarthritis (jSpA) with the HLA-B27 genotype is well established, but there is little knowledge of other genetic factors with a role in disease development. The aim of the present study was to identify and confirm gene signatures and novel biomarkers in various cohorts of untreated and treated patients diagnosed with jSpA and other forms of juvenile idiopathic arthritis (JIA). DNA microarray gene expression was performed in 11 patients with jSpA and in four healthy controls, along with bioinformatics analysis of retrieved data (DAVID, GSEA, IPA). Total RNA was isolated from whole blood of 45 children with known HLA genotype and diagnosis of jSpA according to ILAR criteria, 11 children with oligo- and polyarticular forms of JIA, as well as 12 age and sex matched control participants without diagnosis of chronic inflammatory disease. Of those 11 patient and 4 controls were utilized in the microarrays experiments, while the rest were used in the follow-up qPCR analyses

2014-10-31 | E-GEOD-58667 | biostudies-arrayexpress

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