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Unterberger, C.* ; Staples, K.J.* ; Smallie, T.* ; Williams, L.* ; Foxwell, B.* ; Schaefer, A.* ; Kempkes, B. ; Hofer, T.P.* ; Koeppel, M.* ; Lohrum, M.* ; Stunnenberg, H.* ; Frankenberger, M.* ; Ziegler-Heitbrock, L.

Role of STAT3 in glucocorticoid-induced expression of the human IL-10 gene.

Mol. Immunol. 45, 3230-3237 (2008)
DOI
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
In the present report we have determined the molecular mechanisms, which govern the expression of the human IL-10 gene when induced by the glucocorticoid Methyl-Prednisolone (MP). Treatment of cells with MP at 10-6 M will readily induce IL-10 in CD19+ primary B cells and in a human B cell line. Analysis of the IL-10 promoter showed a robust 18-fold induction and demonstrated that a potential GRE motif was not required, while mutation of the -120 STAT-motif strongly reduced MP-induced trans-activation. A strong induction was also seen with a trimeric STAT-motif and over-expression of dominant-negative STAT3 could block MP induction of IL-10 mRNA. Finally, MP treatment induced binding of STAT3 to the promoter as shown by gelshift, supershift and by chromatin-immunoprecipitation. These data show that glucocorticoid-induced expression of the IL-10 gene is mediated by the transcription factor STAT3.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Human; B cells; Cytokines; Inflammation; Transcription factors
ISSN (print) / ISBN 0161-5890
e-ISSN 1872-9142
Zeitschrift Molecular Immunology
Quellenangaben Band: 45, Heft: 11, Seiten: 3230-3237 Artikelnummer: , Supplement: ,
Verlag Elsevier
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) CCG Inflammatory Lung Diseases (CPC-KEL)
Research Unit Gene Vector (AGV)