Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA392732 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6484790_1.fastq.gz | Fastqsanger.gz | |||
| SRR6484790_2.fastq.gz | Fastqsanger.gz | |||
| SRR6484800_1.fastq.gz | Fastqsanger.gz | |||
| SRR6484800_2.fastq.gz | Fastqsanger.gz | |||
| SRR6484791_1.fastq.gz | Fastqsanger.gz |
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Project description:This SuperSeries is composed of the following subset Series: GSE21111: Basal in vitro transcriptomes of Mycobacterium tuberculosis complex (MTC) clinical isolates GSE21112: Intracellular transcriptional adaptation of Mycobacterium tuberculosis complex (MTC) clinical isolates inside resting murine macrophages GSE21113: Intracellular transcriptional adaptation of Mycobacterium tuberculosis complex (MTC) clinical isolates inside activated murine macrophages Refer to individual Series
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Project description:Analysis of Mtb infected murine macrophages derived from C57Bl/6 WT, TPL2KO, IFNARKO & TPL2IFNAR DKO mice [Set 1] Tuberculosis, caused by Mycobacterium tuberculosis (Mtb), remains a leading cause of mortality and morbidity worldwide, causing approximately 1.4 million deaths per year. Key immune components for host protection during tuberculosis include the cytokines IL?12, IL?1 and TNF??, as well as IFN?? and CD4+ Th1 cells. However, immune factors determining whether individuals control infection or progress to active tuberculosis are incompletely understood. Excess amounts of type I interferon have been linked to exacerbated disease during tuberculosis in mouse models and to active disease in patients, suggesting tight regulation of this family of cytokines is critical to host resistance. In addition, the immunosuppressive cytokine IL?10 is known to inhibit the immune response to Mtb in murine models through the negative regulation of key pro-inflammatory cytokines and the subsequent Th1 response. We show here, using a combination of transcriptomic analysis, genetics and pharmacological inhibitors that the TPL-2-ERK1/2 signaling pathway is important in mediating host resistance to tuberculosis through negative regulation of type I interferon production. The TPL-2-ERK1/2 signalling pathway regulated production by macrophages of several cytokines important in the immune response to Mtb as well as regulating induction of a large number of additional genes, many in a type I IFN dependent manner. In the absence of TPL-2 in vivo, excess type I interferon promoted IL-10 production and exacerbated disease. These findings describe an important regulatory mechanism for controlling tuberculosis and reveal mechanisms by which type I interferon may promote susceptibility to this important disease. Macrophages were derived from C57Bl/6 bone marrow, plated and infected with Mtb H37Rv (or not) in duplicate wells. Samples were then harvested for RNA at time 0 (uninfected only), 15m, 30m, 1hr, 3hr, 6hr and 24hr.
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