Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA315881 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3279660_1.fastq.gz | Fastqsanger.gz | |||
| SRR3279660_2.fastq.gz | Fastqsanger.gz | |||
| SRR3279661_1.fastq.gz | Fastqsanger.gz | |||
| SRR3279661_2.fastq.gz | Fastqsanger.gz |
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Project description:<p><b>Introduction</b><br/>Behçet's disease (BD) is a genetically complex multisystem disease of unknown etiology, characterized by recurrent inflammatory attacks affecting orogenital mucosa, eyes, skin, joints, blood vessels, and less frequently, the central nervous system and gastrointestinal tract. Family studies suggest a genetically complex contribution to BD. With the exception of HLA-B51, which explains less than 20% of the genetic risk, the identities of alleles that are responsible for the complex inheritance of this disease have remained unclear.</p> <p><b>Aim</b><br/>To identify genes that contribute to BD susceptibility.</p> <p><b>Methods</b><br/>A genome-wide association study was undertaken with 311,459 informative and high quality SNPs in a collection of 1215 BD patients and 1278 healthy controls from Turkey using a beadchip microarray assay (Infinium SNP genotype assay, Illumina). HLA-B types were determined with a reverse sequence-specific oligonucleotide method (One Lambda). Regions with evidence for association were fine-mapped using Sequenom iPLEX gold assays. Disease-associated SNPs were genotyped in additional ethnically matched case/control collections from diverse genetic backgrounds, including a total of 2430 cases and 2660 controls, using TaqMan SNP genotype assays. Association data were combined in a meta-analysis of all the collections.</p> <p><b>Results</b><br/>We confirmed the known association with HLA-B51 and found evidence for a second, independent susceptibility locus in the Class I region of the MHC. In addition, we identified one SNP with genome-wide evidence for disease association (P < 5.0 x 10<sup>-8</sup>) within the gene encoding the immunoregulatory cytokine, interleukin-10 (IL10). A meta-analysis of the data from all the collections established associations with the IL10 variant (rs1518111, P = 3.54 x 10<sup>-18</sup>, odds ratio 1.45 with 95% confidence interval 1.34 to 1.58) and with a variant located between the interleukin-23 receptor (IL23R) and interleukin 12 receptor β2 (IL12RB2) genes (rs924080, P = 6.69 x 10<sup>-9</sup>, odds ratio 1.28 with 95% confidence interval 1.18 to 1.39). The disease-associated IL10 variant was associated with diminished mRNA expression and low protein production by cells obtained from healthy blood donors.</p> <p><b>Conclusions</b><br/>These data suggest that genetically encoded low production of IL-10 increases risk of BD and suggest novel interventional targets in the IL-10 and IL-23 pathways.</p> <p>Note: The submitted data are the genotypes of the 311,459 SNPs in 1215 cases and 1278 controls.</p>
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Project description:Differential interleukin-10 (IL-10) expression is suspected to contribute to strain specific differences in the course of Theiler's murine encephalomyelitis virus infection in mice. To determine the expression kinetics of IL-10 and related genes, RNA-based next generation sequencing (RNA-seq) was performed with brain cells obtained from infected SJL mice. Methods: 5-week old, female SJL mice were infected with the BeAn strain of TMEV and sacrificed 4, 7 or 14 days post infection (dpi). RNA was isolated from transversal sections of brain tissue at the level of the hippocampus. RNA-seq was performed on an Illumina HiSeq2500 system. Genes involved in Interleukin-10 (IL-10) signalling were analyzed and transcript levels were compared during the course of infection. Results: A significant upregulation of Interleukin-10 (Il10), Interleukin-10 receptor subunit α (ll10rα), Janus kinase 1 (Jak1) and signal transducer and activator of transcription 3 (Stat3) was detected 7 days post infection (dpi) compared to 4 dpi. Same genes showed a significant downregulation at 14 dpi compared to 7 dpi. Suppressor of cytokine signaling 3 (Socs3) was significantly downregulated at 14 dpi compared to 7 dpi. No differences were detected between transcript levels of interleukin-10 receptor subunit β (Il10rβ) and tyrosine kinase 2 (Tyk2). Conclusion: IL-10 pathway gene expression is transiently upregulated following TMEV-infection of SJL-mice.
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