Skin Rashes Research Today is a free monthly online journal that collates and summarizes the latest research about Skin Rashes, including details on dermatitis, itches, creams, medication, treatment.

In vivo transfection of a cis element 'decoy' against signal transducers and activators of the transcription 6 (STAT6) binding site ameliorates the response of contact hypersensitivity.

Sumi K, Yokozeki H, Wu MH, Satoh T, Kaneda Y, Takeda K, Akira S, Nishioka K

Department of Environmental Immunodermatology, Postgraduate School, Tokyo Medical & Dental University, Tokyo, Japan.

We herein demonstrate that STAT6 plays an important role in the induction of not only acute contact hypersensitivity (CHS), but also chronic CHS in a mouse model using STAT6-deficient (STAT6(-/-)) mice. We, therefore, determine whether synthetic double-stranded DNA with a high affinity for STAT6 can be introduced in vivo as a decoy cis element to bind the transcriptional factor and block the induction of not only acute CHS but also chronic CHS. Treatment by the transfection of STAT6 decoy oligodeoxynucleotides (ODN), after the induction of 2,4,6-trinitrochlorobenzene or other haptens had a significant inhibitory effect on the induction of both acute CHS and chronic CHS. We thus examined the mechanism of the in vivo effect of the transfection of STAT6 decoy ODN in both acute and chronic CHS. In the histological analysis, the infiltration of eosinophils and degranulated mast cells, and the production of IL-4, IL-6 and eotaxin, but not IFN-gamma in the extracts from challenged skin significantly decreased by the transfection of STAT6 decoy ODN. We herein report the first successful in vivo transfer of STAT6 decoy ODN to inhibit acute and chronic CHS, thus providing a new therapeutic strategy not only for the treatment of CHS but also for atopic dermatitis.

Published 1 December 2004 in Gene Ther, 11(24): 1763-71.
Full-text of this article is available online (may require subscription).

© 2004-2008 Skin Rashes Research Today. All Rights Reserved.