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    The Gli3 transcription factor expressed in the thymus stroma controls thymocyte negative selection via Hedgehog-dependent and -independent mechanisms

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    Authors
    Hager-Theodorides, Ariadne L.
    Furmanski, Anna L.
    Ross, Susan
    Outram, Susan V.
    Rowbotham, Nicola J.
    Crompton, Tessa
    Issue Date
    2009-08-20
    Subjects
    Hedgehog (Hh)
    C550 Immunology
    
    Metadata
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    Abstract
    The Hedgehog (Hh) responsive transcription factor Gli3 is required for efficient thymocyte development in the fetus. In this study we show that Gli3, not detected in adult thymocytes, is expressed in the murine fetal and adult thymus stroma. PCR array analysis revealed Cxcl9, Rbp1, and Nos2 as novel target genes of Gli3. We show that Gli3 positively regulates the expression of these genes, most likely by suppressing an intermediate repressor. Deletion of autoreactive thymocytes depends on their interactions with the thymus stroma. Repression of the proapoptotic gene Nos2 in Gli3 mutants coincides with reduced apoptosis of double positive thymocytes undergoing negative selection in vitro and in vivo, and the production of autoreactive thymocytes. Taken together these data indicate that Gli3 controls thymocyte apoptosis and negative selection possibly via the regulation of Nos2. Defective Gli3 expression in the thymus stroma also resulted in decreased CD5 expression on mature thymocytes and inappropriate production of MHC class I-selected CD4+ cells, both consistent with reduced TCR signal strength. Overall our data indicate that Gli3 expressed in the thymus stroma regulates negative selection and TCR signal strength via Hh-dependent and -independent mechanisms, with implications for autoimmunity.
    Citation
    Hager-Theodorides AL, Furmanski AL, Ross SE, Outram SV, Rowbotham NJ, Crompton T (2009) 'The Gli3 transcription factor expressed in the thymus stroma controls thymocyte negative selection via Hedgehog-dependent and -independent mechanisms', Journal of Immunology, 183 (5), pp.3023-3032.
    Publisher
    American Association of Immunologists
    Journal
    Journal of Immunology
    URI
    http://hdl.handle.net/10547/623400
    DOI
    10.4049/jimmunol.0900152
    PubMed ID
    19667090
    Additional Links
    http://www.jimmunol.org/cgi/content/full/183/5/3023
    Type
    Article
    Language
    en
    ISSN
    0022-1767
    ae974a485f413a2113503eed53cd6c53
    10.4049/jimmunol.0900152
    Scopus Count
    Collections
    Biomedical and biological science

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