Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA302461 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2920850_1.fastq.gz | Fastqsanger.gz | |||
| SRR2920850_2.fastq.gz | Fastqsanger.gz | |||
| SRR2920860_1.fastq.gz | Fastqsanger.gz | |||
| SRR2920860_2.fastq.gz | Fastqsanger.gz | |||
| SRR2920870_1.fastq.gz | Fastqsanger.gz |
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Project description:Single-cell transcriptional profiling of Th17 cells, harvested at peak of disease in EAE from LN [EAE-LN-IL-17A/GFP+]
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Project description:Extensive cellular heterogeneity exists within specific immune-cell subtypes classified as a single lineage, but its molecular underpinnings are rarely characterized at a genomic scale. Here, we use single-cell RNA-seq to investigate the molecular mechanisms governing heterogeneity and pathogenicity of Th17 cells isolated from the central nervous system (CNS) and lymph nodes (LN) at the peak of autoimmune encephalomyelitis (EAE) or polarized in vitro under either pathogenic or non-pathogenic differentiation conditions. Computational analysis reveals a spectrum of cellular states in vivo, including a self-renewal state, Th1-like effector/memory states and a dysfunctional/senescent state. Relating these states to in vitro differentiated Th17 cells, unveils genes governing pathogenicity and disease susceptibility. Using knockout mice, we validate four novel genes: Gpr65, Plzp, Toso and Cd5l (in a companion paper). Cellular heterogeneity thus informs Th17 function in autoimmunity, and can identify targets for selective suppression of pathogenic Th17 cells while sparing non-pathogenic tissue-protective ones. Single-cell transcriptional profiling of Th17 cells, harvested at peak of disease in EAE from CNS
2015-11-20 | E-GEOD-75107 | biostudies-arrayexpress
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2015-11-20 | E-GEOD-75108 | biostudies-arrayexpress
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Project description:Dysregulated Th17 cell responses underlie multiple inflammatory and autoimmune diseases, including autoimmune uveitis and its animal model, EAU. However, clinical trials targeting IL-17A in uveitis were not successful. Here, we found that Th17 cells were regulated by their own signature cytokine, IL-17A. Loss of IL-17A in autopathogenic Th17 cells did not reduce their pathogenicity and instead elevated their expression of the Th17 cell cytokines GM-CSF and IL-17F. Mechanistic in vitro studies revealed a Th17 cell-intrinsic autocrine loop triggered by binding of IL-17A to its receptor, leading to activation of transcription factor NFκB and induction of IL 24, which repressed the Th17 cytokine program. In vivo, IL-24 treatment ameliorated Th17-induced EAU, whereas silencing of IL-24 in Th17 cells enhanced disease. This regulatory pathway also operated in human Th17 cells. Thus, IL-17A limits pathogenicity of Th17 cells by inducing IL-24. These findings may explain the disappointing therapeutic effect in targeting IL-17A in uveitis.
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Project description:The goal of these studies is to define the molecular signatures of TH1-induced EAE and TH17-induced EAE through adoptive transfer. We will also define the role of IL-17 signaling in the pathology by comparing cells derived from wild type mice to those derived from mice lacking Act1, a key adaptor required for IL-17 dependent signaling. Brains and spinal cords from animals at peak of disease will be profiled.
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Project description:Population transcriptional profiling of Th17 cells, isolated from CNS or LN at peak of disease in EAE
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