Roquin represses autoimmunity by limiting inducible T-cell co-stimulator messenger RNA View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2007-11

AUTHORS

Di Yu, Andy Hee-Meng Tan, Xin Hu, Vicki Athanasopoulos, Nicholas Simpson, Diego G. Silva, Andreas Hutloff, Keith M. Giles, Peter J. Leedman, Kong Peng Lam, Christopher C. Goodnow, Carola G. Vinuesa

ABSTRACT

Immune responses are normally targeted against microbial pathogens and not self-antigens by mechanisms that are only partly understood. Here we define a newly discovered pathway that prevents autoimmunity by limiting the levels on T lymphocytes of aco-stimulatory receptor, the inducible T-cell co-stimulator(ICOS). In sanroque mice homozygous for an M199R mutation in the ROQ domain of Roquin (also known as Rc3h1), increased Icos expression on T cells causes the accumulation of lymphocytes that is associated with a lupus-like autoimmune syndrome. Roquin normally limits Icos expression by promoting the degradation of Icos messenger RNA.A conserved segment in the unusually long ICOS 3' untranslated mRNA is essential for regulation by Roquin. This segment comprises a 47-base-pair minimal region complementary to T-cell-expressed microRNAs including miR-101, the repressive activity of which is disrupted by base-pair inversions predicted to abrogate miR-101 binding. These findings illuminate a critical post-transcriptional pathway within T cells that regulates lymphocyte accumulation and autoimmunity, and highlights the therapeutic potential of partially antagonising the ICOS pathway. More... »

PAGES

299

References to SciGraph publications

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/nature06253

    DOI

    http://dx.doi.org/10.1038/nature06253

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1016533429

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/18172933


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