par Fayyad Kazan, Hussein 
;Rouas, Redouane ;Burny, Arsène ;Martiat, Philippe ;Hamade, Eva;El Zein, Nabil ;ElDirani, Rim;Hussein, Nader;Fakhry, Maya;Al-Akoum, Carine;Badran, Bassam ;Najar, Mehdi ;Fayyad Kazan, Mohammad
Référence Human immunology, 75, 7, page (677-685)
Publication Publié, 2014
;Rouas, Redouane ;Burny, Arsène ;Martiat, Philippe ;Hamade, Eva;El Zein, Nabil ;ElDirani, Rim;Hussein, Nader;Fakhry, Maya;Al-Akoum, Carine;Badran, Bassam ;Najar, Mehdi ;Fayyad Kazan, Mohammad Référence Human immunology, 75, 7, page (677-685)
Publication Publié, 2014
Article révisé par les pairs
| Résumé : | IFN-γ is a cytokine with important roles in the innate and adaptive immune responses. This cytokine is secreted by activated T cells, NK cells and macrophages. Studies on the regulation of human IFN-γ expression had been previously focused on the promoter region. Consequently, the role of microRNAs (miRs) in this regulation has not been investigated yet. As miR-24 and miR-181 were found to have potential target sites in IFN-γ mRNA 3'UTR, we assessed their impact on IFN-γ expression by co-stimulating PB CD4+ T cells with anti-CD3, anti-CD28, IL-12, and IL-18. This co-stimulation cocktail induced an abundant secretion of IFN-γ together with a down-regulation of miR-24, and miR-181. Existence of a link between these two phenomena was further substantiated by transfection and transduction assays that showed that these two miRs negatively regulate IFN-γ expression by directly binding to their target sites in the mRNA. Thus, identifying target sites for miR-24 and miR-181 in IFN-γ-3'UTR points to a novel regulatory mechanism of this crucial gene. © 2014 American Society for Histocompatibility and Immunogenetics. |
