Transcriptional Repressor HIC1 Contributes to Suppressive Function of Human Induced Regulatory T Cells

 |  Login

Show simple item record

dc.contributor Aalto-yliopisto fi
dc.contributor Aalto University en Ubaid Ullah, Ullah Andrabi, Syed Bilal Ahmad Tripathi, Subhash Kumar Dirasantha, Obaiah Kanduri, Kartiek Rautio, Sini Gross, Catharina C. Lehtimäki, Sari Bala, Kanchan Tuomisto, Johanna Bhatia, Urvashi Chakroborty, Deepankar Elo, Laura L. Lähdesmäki, Harri Wiendl, Heinz Rasool, Omid Lahesmaa, Riitta 2018-04-04T09:38:39Z 2018-04-04T09:38:39Z 2018-02-20
dc.identifier.citation Ubaid Ullah , U , Andrabi , S B A , Tripathi , S K , Dirasantha , O , Kanduri , K , Rautio , S , Gross , C C , Lehtimäki , S , Bala , K , Tuomisto , J , Bhatia , U , Chakroborty , D , Elo , L L , Lähdesmäki , H , Wiendl , H , Rasool , O & Lahesmaa , R 2018 , ' Transcriptional Repressor HIC1 Contributes to Suppressive Function of Human Induced Regulatory T Cells ' Cell Reports , vol 22 , no. 8 , pp. 2094-2106 . DOI: 10.1016/j.celrep.2018.01.070 en
dc.identifier.issn 2211-1247
dc.identifier.other PURE UUID: d946adda-9300-4a3c-88c9-08895ecc3d6f
dc.identifier.other PURE ITEMURL:
dc.identifier.other PURE LINK:
dc.identifier.other PURE FILEURL:
dc.description.abstract Regulatory T (Treg) cells are critical in regulating the immune response. In vitro induced Treg (iTreg) cells have significant potential in clinical medicine. However, applying iTreg cells as therapeutics is complicated by the poor stability of human iTreg cells and their variable suppressive activity. Therefore, it is important to understand the molecular mechanisms of human iTreg cell specification. We identified hypermethylated in cancer 1 (HIC1) as a transcription factor upregulated early during the differentiation of human iTreg cells. Although FOXP3 expression was unaffected, HIC1 deficiency led to a considerable loss of suppression by iTreg cells with a concomitant increase in the expression of effector T cell associated genes. SNPs linked to several immune-mediated disorders were enriched around HIC1 binding sites, and in vitro binding assays indicated that these SNPs may alter the binding of HIC1. Our results suggest that HIC1 is an important contributor to iTreg cell development and function. Ullah et al. find that HIC1 is induced during human iTreg cell differentiation. HIC1 binds to and regulates the expression of key genes during iTreg differentiation. Several autoimmune-disease-associated SNPs are enriched near HIC1 ChIP-seq peaks. en
dc.format.extent 13
dc.format.extent 2094-2106
dc.format.mimetype application/pdf
dc.language.iso en en
dc.relation.ispartofseries Cell Reports en
dc.relation.ispartofseries Volume 22, issue 8 en
dc.rights openAccess en
dc.subject.other Biochemistry, Genetics and Molecular Biology(all) en
dc.subject.other 113 Computer and information sciences en
dc.title Transcriptional Repressor HIC1 Contributes to Suppressive Function of Human Induced Regulatory T Cells en
dc.type A1 Alkuperäisartikkeli tieteellisessä aikakauslehdessä fi
dc.description.version Peer reviewed en
dc.contributor.department Åbo Akademi University
dc.contributor.department Department of Computer Science
dc.contributor.department Professorship Lähdesmäki H.
dc.contributor.department University of Münster
dc.subject.keyword ChIP-seq
dc.subject.keyword expression kinetics
dc.subject.keyword FOXP3
dc.subject.keyword HIC1
dc.subject.keyword iTreg
dc.subject.keyword regulatory SNP
dc.subject.keyword RNA-seq
dc.subject.keyword suppression
dc.subject.keyword T cells
dc.subject.keyword transcriptional regulation
dc.subject.keyword Biochemistry, Genetics and Molecular Biology(all)
dc.subject.keyword 113 Computer and information sciences
dc.identifier.urn URN:NBN:fi:aalto-201804042069
dc.identifier.doi 10.1016/j.celrep.2018.01.070
dc.type.version publishedVersion

Files in this item

Files Size Format View

There are no open access files associated with this item.

This item appears in the following Collection(s)

Show simple item record

Search archive

Advanced Search

article-iconSubmit a publication