Retinoid X receptor ablation in adult mouse keratinocytes generates an atopic dermatitis triggered by thymic stromal lymphopoietin.

Fiche publication


Date publication

octobre 2005

Journal

Proceedings of the National Academy of Sciences of the United States of America

Auteurs

Membres identifiés du Cancéropôle Est :
Pr CHAMBON Pierre, Dr METZGER Daniel, Dr TELETIN Marius


Tous les auteurs :
Li M, Messaddeq N, Teletin M, Pasquali JL, Metzger D, Chambon P

Résumé

To investigate the role of retinoid X receptors (RXRs) in epidermal homeostasis, we generated RXRalphabeta(ep-/-) somatic mutants in which both RXRalpha and RXRbeta are selectively ablated in epidermal keratinocytes of adult mice. These mice develop a chronic dermatitis mimicking that observed in atopic dermatitis (AD) patients. In addition, they exhibit immunological abnormalities including elevated serum levels of IgE and IgG, associated with blood and tissue eosinophilia, indicating that keratinocyte-selective ablation of RXRs also generates a systemic syndrome similar to that found in AD patients. Furthermore, the profile of increased expression of cytokines and chemokines in skin of keratinocyte-selective RXRalphabeta-ablated mutants was typical of a T helper 2-type inflammation, known to be crucially involved in human AD pathogenesis. Finally, we demonstrate that thymic stromal lymphopoietin, whose expression is rapidly and strongly induced in RXRalphabeta-ablated keratinocytes, plays a key role in initiating the skin and systemic AD-like pathologies.

Mots clés

Animals, Cytokines, metabolism, Dermatitis, Atopic, genetics, Genotype, Immunoglobulin E, blood, Immunoglobulin G, blood, Immunohistochemistry, Keratinocytes, metabolism, Mice, Mice, Knockout, Retinoid X Receptors, genetics, Skin, metabolism

Référence

Proc. Natl. Acad. Sci. U.S.A.. 2005 Oct;102(41):14795-800