My NCBISign In

Display Settings:

Format

Send to:

Choose Destination
    J Immunol. 2006 May 1;176(9):5161-6.

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

    Grenningloh R, Gho A, di Lucia P, Klaus M, Bollag W, Ho IC, Sinigaglia F, Panina-Bordignon P.

    Source

    Bioxell SpA, Milan, Italy. rgrenningloh@rics.bwh.harvard.edu

    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-gamma 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.

    PMID:
    16621979
    [PubMed - indexed for MEDLINE]
    Free full text

    MeSH Terms, Substances

    MeSH Terms

    Substances

    LinkOut - more resources

    Full Text Sources

    Other Literature Sources

    Medical

    Libraries

      Supplemental Content

      Icon for HighWire Press

      Save items

      loading

      Related citations in PubMed

      See reviews... See all...

      Cited by 8 PubMed Central articles

      See all...

      Related information

      • Related Citations
        Calculated set of PubMed citations closely related to the selected article(s) retrieved using a word weight algorithm. Related articles are displayed in ranked order from most to least relevant, with the “linked from” citation displayed first.
      • Substance (MeSH Keyword)
        PubChem chemical substance (submitted) records that are classified under the same Medical Subject Headings (MeSH) controlled vocabulary as the current articles.
      • Cited in PMC
        Full-text articles in the PubMed Central Database that cite the current articles.

      Recent activity

      Clear Turn Off Turn On

      Your browsing activity is empty.

      Activity recording is turned off.

      Turn recording back on

      See more...
      You are here: NCBI > Literature > PubMed
      Write to the Help Desk