Contrasting effects of IFNalfa on MHC class II expression in professional vs. nonprofessional APCs: Role of CIITA type IV promoter (Articolo in rivista)

Type
Label
  • Contrasting effects of IFNalfa on MHC class II expression in professional vs. nonprofessional APCs: Role of CIITA type IV promoter (Articolo in rivista) (literal)
Anno
  • 2012-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.1016/j.rinim.2012.09.001 (literal)
Alternative label
  • Pisapia L, Del Pozzo G, Barba P, Citro A, Harris P.E, Maffei A. (2012)
    Contrasting effects of IFNalfa on MHC class II expression in professional vs. nonprofessional APCs: Role of CIITA type IV promoter
    in Results in Immunology
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Pisapia L, Del Pozzo G, Barba P, Citro A, Harris P.E, Maffei A. (literal)
Pagina inizio
  • 174 (literal)
Pagina fine
  • 183 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 2 (literal)
Rivista
Note
  • Scopus (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • Institute of Genetics and Biophysics A. Buzzati-Traverso, CNR, Naples, Italy Department of Medicine of Columbia University Medical Center, New York, NY, USA (literal)
Titolo
  • Contrasting effects of IFNalfa on MHC class II expression in professional vs. nonprofessional APCs: Role of CIITA type IV promoter (literal)
Abstract
  • We previously demonstrated that, in ex vivo cultures, IFN? downregulates the expression of MHC class II (MHCII) genes in human non-professional APCs associated with pancreatic islets. IFN? has an opposing effect on MHCII expression in professional APCs. In this study, we found that the mechanism responsible for the IFN?-mediated MHCII's downregulation in human MHCII-positive non-professional antigen presenting human non-hematopoietic cell lines is the result of the negative feedback system that regulates cytokine signal transduction, which eventually inhibits promoters III and IV of CIITA gene. Because the CIITA-PIV isoform is mostly responsible for the constitutive expression of MHCII genes in non-professional APCs, we pursued and achieved the specific knockdown of CIITA-PIV mRNA in our in vitro system, obtaining a partial silencing of MHCII molecules similar to that obtained by IFN?. We believe that our results offer a new understanding of the potential significance of CIITA-PIV as a therapeutic target for interventional strategies that can manage autoimmune disease and allograft rejection with little interference on the function of professional APCs of the immune system. (literal)
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