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1000
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Abstract/Summary
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<jats:p>CD8<jats:sup>+</jats:sup> T cells are involved in the pathogenesis of multiple sclerosis (MS). The interleukin-2 receptor α (IL-2Rα) is important for CD8<jats:sup>+</jats:sup> T cell function, and single nucleotide polymorphisms (SNPs) in the <jats:italic>IL2RA</jats:italic> gene encoding IL-2Rα increase the risk of MS. Therefore, in isolated CD8<jats:sup>+</jats:sup> T cells we investigated <jats:italic>IL2RA</jats:italic> gene methylation and gene expression in relation to the MS-associated <jats:italic>IL2RA</jats:italic> SNP rs2104286 and soluble IL-2Rα (sIL-2Rα). We have identified allele specific methylation of the CpG-site located in intron 1 that is perturbed by the rs2104286 SNP in CD8<jats:sup>+</jats:sup> T cells from genotype-selected healthy subjects (HS). However, methylation of selected CpG-sites in the promotor or 5’UTR region of the <jats:italic>IL2RA</jats:italic> gene was neither associated with the rs2104286 SNP nor significantly correlated with <jats:italic>IL2RA</jats:italic> gene expression in HS. In CD8<jats:sup>+</jats:sup> T cells from HS, we explored expression of immune relevant genes but observed only few associations with the rs2104286 SNP. However, we found that sIL-2Rα correlated negatively with expression of 55 immune relevant genes, including the IL-7 receptor gene, with Spearman’s rho between -0.49 and -0.32. Additionally, in HS by use of flow cytometry we observed that the IL-7 receptor on naïve CD8<jats:sup>+</jats:sup> T cells correlated negatively with sIL-2Rα and was downregulated in carriers of the rs2104286 MS-associated risk genotype. Collectively, our study of resting CD8<jats:sup>+</jats:sup> T cells indicates that the rs2104286 SNP has a minor effect and sIL-2Rα may negatively regulate the CD8<jats:sup>+</jats:sup> T cell response.</jats:p>
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1000
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Hinweis
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DeepGreen-ID: aefa09c590114ef6b27702d748fc3fda ; metadata provieded by: DeepGreen (https://www.oa-deepgreen.de/api/v1/), LIVIVO search scope life sciences (http://z3950.zbmed.de:6210/livivo), Crossref Unified Resource API (https://api.crossref.org/swagger-ui/index.html), to.science.api (https://frl.publisso.de/), ZDB JSON-API (beta) (https://zeitschriftendatenbank.de/api/), lobid - Dateninfrastruktur für Bibliotheken (https://lobid.org/resources/search)
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