Cutting edge: Inhibition of the retinoid X receptor (RXR) blocks T helper 2 differentiation and prevents allergic lung inflammation

Roland Grenningloh, Andrea Gho, Pietro Di Lucia, Michael Klaus, Werner Bollag, I. Cheng Ho, Francesco Sinigaglia, Paola Panina-Bordignon

Research output: Contribution to journalArticlepeer-review

Abstract

Among the many factors regulating Th cell differentiation, some nuclear hormone receptors are emerging as important players. The retinoid X receptor (RXR) functions as heterodimerization partner for a variety of nuclear hormone receptors. We show in this study that RXR is critical for Th2-mediated immunity. An RXR antagonist inhibited Th2 differentiation, resulting in reduced production of IL-4, IL-10, and IL-13, whereas IFN-γ production was enhanced. This effect was dependent on the presence of APCs. In addition, IL-5 production was blocked directly in Th cells. In vivo, inhibition of RXR prevented experimentally induced allergic lung inflammation. Th1-mediated inflammation was not affected. Its specific role in Th2-mediated inflammation makes RXR a promising target for the development of therapies against diseases such as allergic asthma and atopic dermatitis.

Original languageEnglish
Pages (from-to)5161-5166
Number of pages6
JournalJournal of Immunology
Volume176
Issue number9
Publication statusPublished - May 1 2006

ASJC Scopus subject areas

  • Immunology

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