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Next Generation Sequencing for Quantitative Transcriptomic Profiling of TLR7 deficiency in Neurons

ABSTRACT: Next Generation Sequencing for Quantitative Transcriptomic Profiling of TLR7 deficiency in Neurons

PROVIDER: PRJNA472753 | ENA |

REPOSITORIES: ENA

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Next Generation Sequencing for Quantitative Transcriptomic Profiling of TLR7 deficiency in Neurons

Project description:The goal of this study is to compare gene expression of mouse cultured cortical and hippocampal neurons in response of TLR7 defiency at mature stage

2018-06-11 | GSE114814 | GEO

Next Generation Sequencing for Quantitative Transcriptomic Profiling of TLR3, TLR7 and TLR8 Activation in Neurons

Project description:The goal of this study is to compare gene expression of mouse cultured cortical and hippocampal neurons in response to TLR3, TLR7 and TLR8 activation

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Next Generation Sequencing for Quantitative Transcriptomic Profiling of TLR3, TLR7 and TLR8 Activation in Neurons

Project description:Next Generation Sequencing for Quantitative Transcriptomic Profiling of TLR3, TLR7 and TLR8 Activation in Neurons

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Next Generation Sequencing for Quantitative Transcriptomic Profiling of TLR3 and TLR7 activation in Bone-marrow-derived macrophage

Project description:The goal of this study is to compare gene expression between TLR3 and TLR7

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BCR repertoire analysis by Next-generation sequencing of lymphocytes harvested from mice vaccinated with liposomal TLR4 and TLR7 agonists

Project description:BALB/c mice were vaccinated with inactivated influenza A virus adjuvanted with liposomal TLR4 (2B182C) and TLR7 agonists (2B182C) on days 0 and 21. To examine whether the liposomal combined adjuvant increase BCR diversity, lymphocytes in the draining lymph nodes harvested on day 28 were analyzed using next-generation RNA sequencing technology.

2021-03-01 | E-MTAB-8870 | biostudies-arrayexpress

TLR7 ligation augments hematopoiesis in Rps14 deficiency via paradoxical inflammatory signalling

Project description:TLR7 ligation augments hematopoiesis in Rps14 deficiency via paradoxical inflammatory signalling

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X-linked recessive TLR7 deficiency in 1% of men under 60 years with life-threatening COVID-19

Project description:Autosomal inborn errors of type I IFN immunity and autoantibodies against these cytokines underlie at least 10% of critical COVID-19 pneumonia cases. We report very rare, biochemically deleterious X-linked TLR7 variants in 16 unrelated male individuals aged 7 to 71 years (mean: 36.7 years) from a cohort of 1,202 male patients aged 0.5 to 99 years (mean: 52.9 years) with unexplained critical COVID-19 pneumonia. None of the 331 asymptomatically or mildly infected male individuals aged 1.3 to 102 years (mean: 38.7 years) tested carry such TLR7 variants (p = 3.5 x 10-5). The phenotypes of five hemizygous relatives of index cases infected with SARS-CoV-2 include asymptomatic or mild infection (n=2, 5 and 38 years), or moderate (n=1, 5 years), severe (n=1, 27 years), or critical (n=1, 29 years) pneumonia. Two boys (aged 7 and 12 years) from a cohort of 262 male patients with severe COVID-19 pneumonia (mean: 51.0 years) are hemizygous for a deleterious TLR7 variant. The cumulative allele frequency for deleterious TLR7 variants in the male general population is < 6.5x10-4. We also show that blood B-cell lines and myeloid cell subsets from the patients do not respond to TLR7 stimulation, a phenotype rescued by wild-type TLR7. The patients’ blood plasmacytoid dendritic cells (pDCs) produce low levels of type I IFNs in response to SARS-CoV-2. Overall, X-linked recessive TLR7 deficiency is a highly penetrant genetic etiology of critical COVID-19 pneumonia, in about 1.8% of male patients below the age of 60 years. Human TLR7 and pDCs are essential for protective type I IFN immunity against SARS-CoV-2 in the respiratory tract.

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Next Generation Sequencing for Quantitative Transcriptomic Profiling of TLR3 and TLR7 activation in Bone-marrow-derived macrophage

Project description:Next Generation Sequencing for Quantitative Transcriptomic Profiling of TLR3 and TLR7 activation in Bone-marrow-derived macrophage

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TLR7 ligation augments hematopoiesis in Rps14 deficiency via paradoxical inflammatory signalling

Project description:Myelodysplastic syndrome (MDS) is a haematological malignancy characterised by blood cytopenias and predisposition to acute myeloid leukaemia. We developed a model of MDS using zebrafish using knockout of Rps14, the primary mediator of the anaemia associated with del (5q) MDS. These mutant animals develop bone marrow failure with dysplastic features. We conducted an in vivo small molecule screen to identify compounds that ameliorate the MDS phenotype, identifying imiquimod, an agonist of TLR7. We conducted RNA-seq analysis of both treated and untreated animals to define the mechanism of imiquimod in alleviating anaemia. We find imiquimod alleviates anaemia by promoting haematopoietic stem and progenitor cell expansion and erythroid differentiation, the mechanism of which is dependent on TLR7 ligation. TLR7 activation in this setting paradoxically promoted an anti-inflammatory gene signature suggesting crosstalk between pro-inflammatory pathways endogenous to Rps14 loss and TLR7 pathway activation.

2021-03-12 | GSE168727 | GEO

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