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  • Bruhn, SörenLinköpings universitet,Institutionen för klinisk och experimentell medicin,Hälsouniversitetet,Genepathway, Inc., San Diego, CA, USA (author)

Increased expression of IRF4 and ETS1 in CD4+ cells from patients with intermittent allergic rhinitis

  • Article/chapterEnglish2012

Publisher, publication year, extent ...

  • 2011-09-15
  • John Wiley and Sons,2012
  • printrdacarrier

Numbers

  • LIBRIS-ID:oai:DiVA.org:liu-75112
  • https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-75112URI
  • https://doi.org/10.1111/j.1398-9995.2011.02707.xDOI
  • https://gup.ub.gu.se/publication/151554URI

Supplementary language notes

  • Language:English
  • Summary in:English

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  • Subject category:ref swepub-contenttype
  • Subject category:art swepub-publicationtype

Notes

  • Funding Agencies|European Commission|223367|MultiMod||Swedish Medical Research Council||US National Institutes of Health|P01-DA-015027-01R01-MH-074460-01U01-AA-013512U01-AA-013641-04|US Department of Energy under the EPSCoR Laboratory||
  • Background: The transcription factor (TF) IRF4 is involved in the regulation of Th1, Th2, Th9, and Th17 cells, and animal studies have indicated an important role in allergy. However, IRF4 and its target genes have not been examined in human allergy. Methods: IRF4 and its target genes were examined in allergen-challenged CD4+ cells from patients with IAR, using combined gene expression microarrays and chromatin immunoprecipitation chips (ChIP-chips), computational target prediction, and RNAi knockdowns. Results: IRF4 increased in allergen-challenged CD4+ cells from patients with IAR, and functional studies supported its role in Th2 cell activation. IRF4 ChIP-chip showed that IRF4 regulated a large number of genes relevant to Th cell differentiation. However, neither Th1 nor Th2 cytokines were the direct targets of IRF4. To examine whether IRF4 induced Th2 cytokines via one or more downstream TFs, we combined gene expression microarrays, ChIP-chips, and computational target prediction and found a putative intermediary TF, namely ETS1 in allergen-challenged CD4+ cells from allergic patients. ETS1 increased significantly in allergen-challenged CD4+ cells from patients compared to controls. Gene expression microarrays before and after ETS1 RNAi knockdown showed that ETS1 induced Th2 cytokines as well as disease-related pathways. Conclusions: Increased expression of IRF4 in allergen-challenged CD4+ cells from patients with intermittent allergic rhinitis leads to activation of a complex transcriptional program, including Th2 cytokines.

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Added entries (persons, corporate bodies, meetings, titles ...)

  • Barrenäs, FredrikLinköpings universitet,Institutionen för klinisk och experimentell medicin,Hälsouniversitetet(Swepub:gu)xbarfr (author)
  • Mobini, Reza,1965Östergötlands Läns Landsting(Swepub:gu)xmobre (author)
  • Andersson, Bengt A.,1952Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för mikrobiologi och immunologi,Institute of Biomedicine, Department of Microbiology and Immunology,Sahlgrenska University Hospital(Swepub:gu)xabeng (author)
  • Chavali, SreenivasMRC Lab Molecular Biol, Cambridge, UK(Swepub:gu)xchasr (author)
  • Egan, B. S.Genepathway, Inc., San Diego, CA, USA (author)
  • Hovig, E.Norwegian Radium Hospital (author)
  • Sandve, G. K.University of Oslo (author)
  • Langston, M. A.University of Tennessee, Knoxville, TN, USA (author)
  • Rogers, G.University of Tennessee, Knoxville, TN, USA (author)
  • Wang, HuiLinköpings universitet,Institutionen för klinisk och experimentell medicin,Hälsouniversitetet(Swepub:liu)huiwa84 (author)
  • Benson, MikaelLinköpings universitet,Hälsouniversitetet,Pediatrik(Swepub:gu)xbenmi (author)
  • Linköpings universitetInstitutionen för klinisk och experimentell medicin (creator_code:org_t)

Related titles

  • In:Allergy. European Journal of Allergy and Clinical Immunology: John Wiley and Sons67:1, s. 33-400105-45381398-9995

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