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    Leishmania donovani-induced expression of signal regulatory protein alpha on Kupffer cells enhances hepatic invariant NKT-cell activation

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    Author
    Beattie, L; Svensson, M; Bune, A; Brown, N; Maroof, A; Zubairi, S; Smith, KR; Kaye, PM
    Date
    2010-01-01
    Source Title
    European Journal of Immunology
    Publisher
    WILEY
    University of Melbourne Author/s
    Beattie, Lynette
    Affiliation
    Microbiology and Immunology
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Beattie, L., Svensson, M., Bune, A., Brown, N., Maroof, A., Zubairi, S., Smith, K. R. & Kaye, P. M. (2010). Leishmania donovani-induced expression of signal regulatory protein alpha on Kupffer cells enhances hepatic invariant NKT-cell activation. EUROPEAN JOURNAL OF IMMUNOLOGY, 40 (1), pp.117-123. https://doi.org/10.1002/eji.200939863.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/253366
    DOI
    10.1002/eji.200939863
    Abstract
    Signal regulatory protein alpha (SIRPalpha) and its cognate ligand CD47 have been documented to have a broad range of cellular functions in development and immunity. Here, we investigated the role of SIRPalpha-CD47 signalling in invariant NKT (iNKT) cell responses. We found that CD47 was required for the optimal production of IFN-gamma from splenic iNKT cells following exposure to the alphaGalCer analogue PBS-57 and in vivo infection of mice with Leishmania donovani. Surprisingly, although SIRPalpha was undetectable in the liver of uninfected mice, the hepatic iNKT-cell response to infection was also impaired in CD47-/- mice. However, we found that SIRPalpha was rapidly induced on Kupffer cells following L. donovani infection, via a mechanism involving G-protein-coupled receptors. Thus, we describe a novel amplification pathway affecting cytokine production by hepatic iNKT cells, which may facilitate the breakdown of hepatic tolerance after infection.

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