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Interferon-γ signaling in the progression from early to end stage kidney disease in type 2 diabetes

ABSTRACT: Interferon-γ signaling in the progression from early to end stage kidney disease in type 2 diabetes

PROVIDER: PRJNA962837 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24334704_1.fastq.gz	Fastqsanger.gz
	SRR24334704_2.fastq.gz	Fastqsanger.gz
	SRR24334705_1.fastq.gz	Fastqsanger.gz
	SRR24334705_2.fastq.gz	Fastqsanger.gz
	SRR24334706_1.fastq.gz	Fastqsanger.gz

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Interferon-γ signaling in the progression from early to end stage kidney disease in type 2 diabetes

Project description:The effects of circulating pro-inflammatory factors on diabetic kidney disease (DKD) progression remain poorly defined. In this study, transcriptional and proteomic profiling of kidney tissue and blood samples from individuals with type 2 diabetes mellitus and early DKD was used to identify gene expression associated with kidney disease progression. Interferon gamma (IFNG) was both identified as an upstream regulator of gene expression and detected in the serum of individuals who progressed. Individual IFNG activation scores (representing summary expression of 72 downstream signaling mediators) early in disease correlated with DKD progression over an average of 9.7 years. IFNG pathway inhibition reduced gene activity associated with DKD progression in both kidney organoids generated from human pluripotent stem cells and mouse DKD models. Thus, expression of genes associated with IFNG activity early in DKD predicted disease progression; individuals demonstrating IFNG activity may benefit from targeted therapeutics early in the disease course.

2024-05-13 | GSE230848 | GEO

Interferon-γ-dependent regulatory circuits in immune inflammation highlighted in diabetes

Project description:We demonstrate diverse roles of interferon–gamma (IFN-γ) in the induction and regulation of immune-mediated inflammation using a transfer model of autoimmune diabetes. The diabetogenic CD4+BDC2.5 (BDC) T cell clone upon transfer into NOD.scid mice induced destruction of islets of Langerhans leading to diabetes. Administration of a neutralizing antibody to IFN-γ (H22) resulted in long term protection (LTP) from diabetes, with inflammation but persistence of a significant, albeit decreased numbers of β-cells. BDC T cells were a mixture of cells expressing high, intermediate and low levels of the T cell receptor. Clonotype-low BDC T cells were required for LTP. Furthermore, islet infiltrating leukocytes in the LTP mice contained Foxp3+CD4 T cells. Islet inflammation in both diabetic and LTP mice was characterized by heavy infiltration of macrophages. Gene expression profiles indicated that macrophages in diabetic mice were M1-type, while LTP mice contained M2-differentiated. The LTP was abolished if mice were treated with either an antibody depleting CD4 T cells, or a neutralizing antibody to CTLA-4, in this case, only at a late stage. Neutralization of IL-10, TGF-β, GITR or CD25 had no effect. Transfer of only clonotype-high expressing BDC T cells induced diabetes but in contrast, H22 antibodies did not inhibit diabetes. While clonotype high T cells induced diabetes even when IFN-γ was neutralized, paradoxically, there was reduced inflammation and no diabetes if host myeloid cells lacked IFN-γ receptor. Hence, using monoclonal CD4 T cells, IFN-γ can have a wide diversity of roles, depending on the setting of the immune process.

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Project description:Monocyte derived macrophages were exposed to arachidonic acid, interferon beta, or interferon gamma

2021-12-31 | E-MTAB-10867 | biostudies-arrayexpress

Pre-analytical considerations in quantifying circulating miRNAs that predict end-stage kidney disease in diabetes

Project description:Our previous study identified 8 risk and 9 protective plasma miRNAs associated with progression to end-stage kidney disease (ESKD) in diabetes. This study aimed to elucidate pre-analytical factors that influence the quantification of circulating miRNAs. Using the EdgeSeq platform, which quantifies 2,002 miRNAs in plasma, including ESKD-associated miRNAs, we compared miRNA profiles in whole plasma vs. miRNAs profiles in RNA extracted from the same plasma specimens. Less than half of the miRNAs were detected in standard RNA extracted methods from plasma. Detection of individual and concentrations of miRNAs were much lower when RNA extracted from plasma was quantified by RNA sequencing (RNASeq) or RT-qPCR platforms compared to EdgeSeq. Plasma profiles of miRNAs determined by the EdgeSeq platform had excellent reproducibility in assessment, and had no variation with age, sex, HbA1c, BMI, and cryostorage time. The risk ESKD-associated miRNAs were detected and measured accurately only in whole plasma and using the EdgeSeq platform. Protective ESKD-associated miRNAs were detected by all platforms except RT-qPCR, however, correlations among concentrations obtained with different platforms were weak or non-existent. In conclusion, pre-analytical factors have a profound effect on detection and quantification of circulating miRNAs in ESKD in diabetes. Quantification of miRNAs in whole plasma and using the EdgeSeq platform may be the preferable method to study profiles of circulating cell-free miRNAs associated with ESKD, and possibly other diseases.

2024-05-07 | GSE266819 | GEO

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Project description:sequencing of the Manx Shearwater Interferon gamma gene

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Project description:Human fibroblasts were infected or not with Toxoplasma gondii (Pru strain) for 18 h at a nominal MOI of 3. Cells were subsequently treated with human recombinant interferon gamma (0.5 ng/ml = 30 pM) for 0, 2, 4 and 8 h before RNA was harvested for cDNA microarray experiments. Uninfected samples were named N0, N2, N4 and N8 (i.e., N2 indicated uninfected cells treated with interferon gamma for 2 h); infected samples were named P0, P2, P4 and P8. Duplicate cultures were analyzed for each condition (indicated as "a" and "b"). The reference channel (ch1, green) contained Universal Human Reference RNA. Using a genome-wide microarray analysis we show here a complete dysregulation of interferon-gamma-inducible gene expression in human fibroblasts infected with Toxoplasma. Notably, 46 of the 127 interferon-gamma-responsive genes were induced and 19 were suppressed in infected cells before they were exposed to interferon gamma, indicating that other stimuli produced during infection may also regulate these genes. Following interferon-gamma treatment, none of the 127 interferon-gamma-responsive genes could be significantly induced in infected cells.

2007-06-06 | E-SMDB-3827 | biostudies-arrayexpress

Expression data from HeLa cells upon interferon-gamma or interferon-beta treatment

Project description:Immune interferon beta and gamma are essential for mammalian host defence against intracellular pathogens. We used microarrays to detail the global programme of gene expression upon interferon-gamma or interferon-beta treatment and identified distinct classes of up-regulated genes.

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Conserved interferon-gamma signaling and decreased immune exclusion programs in responses to immune checkpoint blockade therapy

Project description:We analyzed baseline and on-therapy tumor biopsies from 101 patients with advanced melanoma treated with nivolumab (anti-PD-1) alone or combined with ipilimumab (anti-CTLA-4). Analysis of whole transcriptome data showed that T cell infiltration and interferon-gamma signaling signatures corresponded most highly with clinical response to therapy, with a reciprocal decrease in cell cycle and WNT signaling pathways in responding biopsies. Clinical outcome differences were likely not due to differential melanoma cell responses to interferon-gamma, as 57 human melanoma cell lines exposed in vitro to this cytokine showed a conserved interferon-gamma transcriptome response unless they had mutations that precluded signaling from the interferon-gamma receptor. Therefore, the magnitude of the antitumor T cell response and the corresponding downstream interferon-gamma signaling are the main drivers of clinical response or resistance to immune checkpoint blockade therapy.

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Pre-analytical considerations in quantifying circulating miRNAs that predict end-stage kidney disease in diabetes

Project description:Pre-analytical considerations in quantifying circulating miRNAs that predict end-stage kidney disease in diabetes

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RNA-seq of mouse intestinal organoids treated with interferon-gamma

Project description:We aimed to investigate gene expression changes in intestinal organoids from different mouse genotypes after treatment with interferon-gamma. Wild-type, villinCreER;KrasG12D/+;Trp53fl/flRosa26N1icd/+ (KPN), and villinCreER;Apcfl/fl;KrasG12D/+;Trp53fl/flTgfbrIfl/fl (AKPT) intestinal organoids were plated, and the media was supplemented with 1 ng/mL of recombinant mouse interferon-gamma protein on Day 3. RNA was collected 24h later and processed for RNA sequencing.

2022-06-30 | E-MTAB-11769 | biostudies-arrayexpress

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