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Sökning: onr:"swepub:oai:DiVA.org:uu-383152" > Interferon signatur...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00005009naa a2200529 4500
001oai:DiVA.org:uu-383152
003SwePub
008190510s2019 | |||||||||||000 ||eng|
024a urn:nbn:se:uu:diva-3831522 urn
024a https://doi.org/10.1002/eji.2018479552 DOI
040 a (SwePub)uu
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
100a Kaleviste, Eppu Univ Tartu, Inst Biomed & Translat Med, Dept Biomed, Tartu, Estonia4 aut
2451 0a Interferon signature in patients with STAT1 gain-of-function mutation is epigenetically determined
264 1b WILEY,c 2019
338 a print2 rdacarrier
520 a STAT1 gain-of-function (GOF) variants lead to defective Th17 cell development and chronic mucocutaneous candidiasis (CMC), but frequently also to autoimmunity. Stimulation of cells with STAT1 inducing cytokines like interferons (IFN) result in hyperphosphorylation and delayed dephosphorylation of GOF STAT1. However, the mechanism how the delayed dephosphorylation exactly causes the increased expression of STAT1-dependent genes, and how the intracellular signal transduction from cytokine receptors is affected, remains unknown. In this study we show that the circulating levels of IFN-alpha were not persistently elevated in STAT1 GOF patients. Nevertheless, the expression of interferon signature genes was evident even in the patient with low or undetectable serum IFN-alpha levels. Chromatin immunoprecipitation (ChIP) experiments revealed that the active chromatin mark trimethylation of lysine 4 of histone 3 (H3K4me3), was significantly enriched in areas associated with interferon-stimulated genes in STAT1 GOF cells in comparison to cells from healthy donors. This suggests that the chromatin binding of GOF STAT1 variant promotes epigenetic changes compatible with higher gene expression and elevated reactivity to type I interferons, and possibly predisposes for interferon-related autoimmunity. The results also suggest that epigenetic rewiring may be responsible for treatment failure of Janus kinase 1/2 (JAK1/2) inhibitors in certain patients.
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Immunology in the medical area0 (SwePub)301102 hsv//eng
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Immunologi inom det medicinska området0 (SwePub)301102 hsv//swe
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaper0 (SwePub)3012 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicine0 (SwePub)3012 hsv//eng
653 a autoimmunity
653 a chronic mucocutaneous candidiasis
653 a epigenetics
653 a STAT1 gain-of-function mutation
653 a type I interferon
700a Saare, Mariou Univ Tartu, Inst Biomed & Translat Med, Dept Biomed, Tartu, Estonia4 aut
700a Leahy, Timothy Ronanu Our Ladys Childrens Hosp, Dept Paediat Immunol & Infect Dis, Dublin, Ireland4 aut
700a Bondet, Vincentu Inst Pasteur, INSERM, U1223, Immunobiol Dendrit Cells Unit, Paris, France4 aut
700a Duffy, Darraghu Inst Pasteur, INSERM, U1223, Immunobiol Dendrit Cells Unit, Paris, France4 aut
700a Mogensen, Trine H.u Aarhus Univ Hosp, Dept Infect Dis, Aarhus, Denmark;Aarhus Univ, Dept Biomed, Aarhus, Denmark;Aarhus Univ, Dept Clin Med, Aarhus, Denmark4 aut
700a Jörgensen, Sofie E.u Aarhus Univ, Dept Biomed, Aarhus, Denmark4 aut
700a Nurm, Helkeu Tallinn Childrens Hosp, Dept Emergency Care & Acute Infect, Tallinn, Estonia4 aut
700a Ip, Winnieu Great Ormond St Hosp Sick Children, London, England;UCL Great Ormond St Inst Child Hlth, London, England4 aut
700a Davies, E. Grahamu Great Ormond St Hosp Sick Children, London, England;UCL Great Ormond St Inst Child Hlth, London, England4 aut
700a Sauer, Saschau Max Planck Inst Mol Genet, Otto Warburg Lab, Berlin, Germany;Max Delbruck Ctr Mol Med, BIMSB, BIH, Lab Funct Genom Nutrigen & Syst Biol, Berlin, Germany4 aut
700a Syvänen, Ann-Christine,d 1950-u Uppsala universitet,Molekylär medicin,Science for Life Laboratory, SciLifeLab4 aut0 (Swepub:uu)anncsyva
700a Milani, Liliu Univ Tartu, Estonian Genome Ctr, Tartu, Estonia4 aut
700a Peterson, Pärtu Univ Tartu, Inst Biomed & Translat Med, Dept Biomed, Tartu, Estonia4 aut
700a Kisand, Kaiu Univ Tartu, Inst Biomed & Translat Med, Dept Biomed, Tartu, Estonia4 aut
710a Univ Tartu, Inst Biomed & Translat Med, Dept Biomed, Tartu, Estoniab Our Ladys Childrens Hosp, Dept Paediat Immunol & Infect Dis, Dublin, Ireland4 org
773t European Journal of Immunologyd : WILEYg 49:5, s. 790-800q 49:5<790-800x 0014-2980x 1521-4141
8564 8u http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-383152x lärosäteslänky Till lärosätets (uu) databas
8564 8u https://doi.org/10.1002/eji.201847955

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