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    A requirement for CD45 distinguishes Ly49D-mediated cytokine and chemokine production from killing in primary natural killer cells

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    Author
    Huntington, ND; Xu, YK; Nutt, SL; Tarlinton, DM
    Date
    2005-05-02
    Source Title
    Journal of Experimental Medicine
    Publisher
    ROCKEFELLER UNIV PRESS
    University of Melbourne Author/s
    Nutt, Stephen; Huntington, Nicholas
    Affiliation
    Medical Biology (W.E.H.I.)
    Metadata
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    Document Type
    Journal Article
    Citations
    Huntington, N. D., Xu, Y. K., Nutt, S. L. & Tarlinton, D. M. (2005). A requirement for CD45 distinguishes Ly49D-mediated cytokine and chemokine production from killing in primary natural killer cells. JOURNAL OF EXPERIMENTAL MEDICINE, 201 (9), pp.1421-1433. https://doi.org/10.1084/jem.20042294.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/258039
    DOI
    10.1084/jem.20042294
    Abstract
    Engagement of receptors on the surface of natural killer (NK) cells initiates a biochemical cascade ultimately triggering cytokine production and cytotoxicity, although the interrelationship between these two outcomes is currently unclear. In this study we investigate the role of the cell surface phosphatase CD45 in NK cell development and intracellular signaling from activating receptors. Stimulation via the major histocompatibility complex I-binding receptor, Ly49D on CD45(-/-) primary NK cells resulted in the activation of phosphoinositide-3-kinase and normal cytotoxicity but failed to elicit a range of cytokines and chemokines. This blockage is associated with impaired phosphorylation of Syk, Vav1, JNK, and p38, which mimics data obtained using inhibitors of the src-family kinases (SFK). These data, supported by analogous findings after CD16 and NKG2D stimulation of CD45(-/-) primary NK cells, place CD45 upstream of SFK in NK cells after stimulation via immunoreceptor tyrosine-based activation motif-containing receptors. Thus we identify CD45 as a pivotal enzyme in eliciting a precise subset of NK cell responses.

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