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A non‐classical ISRE/ISGF3 pathway mediates induction of RANTES gene transcription by type I IFNs

I. Cremer,J. Ghysdael,V. Vieillard

Published 2002 in FEBS Letters

ABSTRACT

RANTES (regulated upon activation normal T cell expressed and secreted) is a chemoattractant cytokine important in the generation of inflammatory responses and human immunodeficiency virus resistance. In hematopoietic cells, RANTES is over‐expressed by type I interferons (IFN‐α and IFN‐β). The upstream region of the RANTES gene promoter contains a distal low affinity IFN‐stimulated response element (ISRE). Specific mutagenesis in this ISRE‐like motif abolished the activation of RANTES transcription by type I IFNs. Examination of the ISRE binding factors strongly suggested that signal transducer and activator of transcription (Stat)‐2 and p48/IFN‐stimulated gene factor 3γ (ISGF3γ) are not required for the induction of RANTES by type I IFNs. The specific requirement of Stat‐1 was demonstrated using Stat‐1‐deficient U3A cells. These results revealed a non‐classical ISRE/ISGF3 signal transduction pathway for the induction of RANTES by type I IFNs.

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