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Targeting STAT6 in Atopic Eczema/Dermatitis

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Allergy Frontiers: Future Perspectives

Part of the book series: Allergy Frontiers ((ALLERGY,volume 6))

Abstract

Although considerable progress has been made in elucidating the mechanism of atopoic dermatitis [AD], the cellular and molecular mechanisms regulating AD still remains obscure. Recently, IgE mediated late phase reaction is thought to be mainly associated with the pathogenesis of AD. We have established the eczematous skin reaction induced by anti-DNP-IgE antibody and DNFB in AD model mouse. STAT6 is known as a regulator of IL-4- dependent immune responses. We have also established STAT6 deficient mice and concluded that STAT6 plays a crucial role in exerting IL-4 and IL-13 mediated biological responses. On the basis of these earlier studies, we have developed novel therapy for AD using STAT6 Decoy ODN that clearly downregulated late phase cutaneous response of IgE mediated biphasic reactions, which is now thought to be closely related to skin reactions seen in human AD. Although a number of important issues, such as the safety and side effects, have not yet been addressed in this study, the decoy strategy against STAT6 may provide a new therapeutic modality as gene therapy against AD. In a preliminary study, we applied STAT6 decoy ointment to the refractory AD after ethical approval. Significant improvements of skin scores and pruritis were obtained in four cases. Large scale clinical studies are under way and will provide much more information about the proper clinical use, indications and side effects and usefulness in daily clinical practice in the near future

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Correspondence to Ichiro Katayama .

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Katayama, I., Murota, H., Igawa, K., Satoh, T., Nishioka, K., Yokozeki, H. (2010). Targeting STAT6 in Atopic Eczema/Dermatitis. In: Pawankar, R., Holgate, S.T., Rosenwasser, L.J. (eds) Allergy Frontiers: Future Perspectives. Allergy Frontiers, vol 6. Springer, Tokyo. https://doi.org/10.1007/978-4-431-99365-0_10

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  • DOI: https://doi.org/10.1007/978-4-431-99365-0_10

  • Publisher Name: Springer, Tokyo

  • Print ISBN: 978-4-431-99364-3

  • Online ISBN: 978-4-431-99365-0

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