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Assessment of the impact of the TLR3 L412F variant in terms of TLR3-sensitive transcript induction

ABSTRACT: Assessment of the impact of the TLR3 L412F variant in terms of TLR3-sensitive transcript induction

PROVIDER: PRJNA892959 | ENA |

REPOSITORIES: ENA

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Assessment of the impact of the TLR3 L412F variant in terms of TLR3-sensitive transcript induction

Project description:we assessed the impact of TLR3 L412F at endogenous cellular levels upon double stranded RNA (dsRNA) stimulation, by performing RNA-sequencing in primary fibroblasts from individuals homozygous for the ancestral allele (n =2) or homozygous for TLR3 L412F (n = 4) upon extracellular Poly(I:C) stimulation that activates the TLR3 pathway. The average response of TLR3 L412F homozygotes was significantly decreased (mean Δ log2 fold-change = 0.93; Wilcoxon p <10-16) compared to that of cells with the ancestral allele, approaching that of TLR3-deficient cells, used as negative control.

2023-01-13 | GSE216304 | GEO

Assessment of the impact of the IL23R R381Q variant in terms of IL-23-sensitive transcript induction

Project description:Assessment of the impact of the IL23R R381Q variant in terms of IL-23-sensitive transcript induction

| PRJNA893645 | ENA

Assessment of the impact of the IL23R R381Q variant in terms of IL-23-sensitive transcript induction

Project description:We stimulated T-cell blasts from IL23R R381Q homozygotes (n = 2), healthy controls homozygous for the ancestral allele (n = 9), homozygous individuals for TYK2 P1104A (n = 2) that selectively impairs responses to IL-23, and one patient each with autosomal recessive, complete TYK2 or IL-12Rb1 deficiency with IL-12, IL-23, IL-1b, and IL-1b plus IL-23 for 6 hours and performed RNA-sequencing. We used IL-1b as an IL-23-sensitizing agent as previously reported. We found that while T-cell blasts from IL23R R381Q homozygotes respond normally to IL-12 and IL-1b, their response to IL-23 and to IL-23 plus IL-1b is impaired

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Complete TLR3 deficiency

Project description:The objective of this study is to study the Toll-like receptor 3 (TLR3)-dependent gene expression in human fibroblast cells and peripheral blood mononuclear cells (PBMCs) Fibroblast cells and PBMCs from donors with autosomal recessive (AR) complete TLR3 deficiency and autosomal dominant (AD) partial TLR3 deficiency were collected for microarray analysis to measure the transcriptional responsiveness of TLR3 in fibroblast and PBMCs. A total of 3 healthy controls, 1 AD TLR3-deficient patient, 1 AR TLR3-deficient patient, 1 AR UNC-93B-deficient patient, 1 MyD88 deficient patien were used in this study. The fibroblast cells were cultured in DMEM medium supplemented with 10% fetal calf serum (FCS). The PBMCs were cultured in RPMI medium complemented with 10% FCS. Different kinetics (2 hours and 8 hours) of poly(I:C) (25ug/ml, purchased from Amersham) stimulations were performed, aiming to define TLR3-inducible genes in these human cells. A stimulation of IL-1β (20ng/ml, purchased from R&D system Inc.) was used as a positive activation control with same kinetics of stimulations. A total of one million cells per stimulation were used for fibroblasts, and around 1.5 million cells per stimulation for PBMCs.

2011-11-02 | E-GEOD-30951 | biostudies-arrayexpress

Complete TLR3 deficiency

Project description:The objective of this study is to study the Toll-like receptor 3 (TLR3)-dependent gene expression in human fibroblast cells and peripheral blood mononuclear cells (PBMCs)

2011-11-02 | GSE30951 | GEO

microRNA expression profiling of small intestine of Tlr3+/+ and Tlr3-/- mice after total body g-irradiation

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2015-02-01 | E-GEOD-42916 | biostudies-arrayexpress

Assessment of mTOR-Dependent Translational Regulation of Interferon Stimulated Genes

Project description:Type-I interferon (IFN)-induced activation of the mammalian target of rapamycin (mTOR) signaling pathway has been implicated in translational control of mRNAs encoding interferon-stimulated genes (ISGs). However, mTOR-sensitive translatomes commonly include mRNAs with a 5’ terminal oligopyrimidine tract (TOP), such as those encoding ribosomal proteins, but not ISGs. Because these translatomes were obtained under conditions when ISG expression is not induced, we examined the mTOR-sensitive translatome in human WISH cells stimulated with IFNβ. The mTOR inhibitor Torin1 resulted in a repression of global protein synthesis, including that of ISG products, and translation of all but 3 ISG mRNAs (TLR3, NT5C3A, and RNF19B) was not selectively more sensitive to mTOR inhibition. Detailed studies of NT5C3A revealed an IFN-induced change in transcription start site resulting in a switch from a non-TOP to a TOP-like transcript variant and mTOR sensitive translation. Thus, we show that, in the cell model used, translation of the vast majority of ISG mRNAs is not selectively sensitive to mTOR activity and describe an uncharacterized mechanism wherein the 5’-UTR of an mRNA is altered in response to a cytokine, resulting in a shift from mTOR-insensitive to mTOR-sensitive translation.

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Project description:CD8 positive dendritic cell line , stimulated with or without TLR3 ligand polyI:C We used microarray to obtain global gene expression data of TLR3 regulated genes

2015-06-04 | GSE57512 | GEO

Gene profiling in the colon after depletion and activation of TLR3 and TLR7 signals

Project description:TLR3 and TLR7 are critical recognition receptor which reacts with viruses. TLR3 and TLR7 contribute to many immunological pathway. Especially, TLR3 and TLR7 are clearly involved in the regulation of innate immunity in the gut. To identify the downstream target of TLR 3 and TLR7 in the IBD, we carried out microarray. The colon tissues were isolated from four different groups. None-no treatment, after DSS treated, after DSS+antiviral treatment, after DSS+TLR3+7 agonists.

2016-07-05 | E-GEOD-79241 | biostudies-arrayexpress

Liver gene expression profiles of TLR3-/- versus TLR3wt (C57Bl/6) mice

Project description:cDNA was prepared from total liver RNA taken from untreated, 3 months old, TLR3-/- and TLR3wt C57Bl/6 mice cDNA was prepared from total liver RNA taken from untreated, 3 months old, TLR3-/- and TLR3wt C57Bl/6 mice each group contained 3 mice

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