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    Cognate antigen engagement on parenchymal cells stimulates CD8(+) T cell proliferation in situ

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    Author
    Sutherland, RM; Londrigan, SL; Brady, JL; Carrington, EM; Marchingo, JM; Heinzel, S; Hodgkin, PD; Graham, KL; Kay, TW; Zhan, Y; ...
    Date
    2017-04-12
    Source Title
    Nature Communications
    Publisher
    NATURE PUBLISHING GROUP
    University of Melbourne Author/s
    Graham, Kate; Londrigan, Sarah; Carrington, Emma; Marchingo, Julia; Heinzel, Susanne; Lew, Andrew; Kay, Thomas; Sutherland, Robyn; Hodgkin, Philip; Brady, Jamie; ...
    Affiliation
    Medical Biology (W.E.H.I.)
    Medicine and Radiology
    Microbiology and Immunology
    Metadata
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    Document Type
    Journal Article
    Citations
    Sutherland, R. M., Londrigan, S. L., Brady, J. L., Carrington, E. M., Marchingo, J. M., Heinzel, S., Hodgkin, P. D., Graham, K. L., Kay, T. W., Zhan, Y. & Lew, A. M. (2017). Cognate antigen engagement on parenchymal cells stimulates CD8(+) T cell proliferation in situ. NATURE COMMUNICATIONS, 8 (1), https://doi.org/10.1038/ncomms14809.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/259146
    DOI
    10.1038/ncomms14809
    Abstract
    T-cell responses are initiated upon cognate presentation by professional antigen presenting cells in lymphoid tissue. T cells then migrate to inflamed tissues, but further T-cell stimulation in these parenchymal target sites is not well understood. Here we show that T-cell expansion within inflamed tissues is a distinct phase that is neither a classical primary nor classical secondary response. This response, which we term 'the mezzanine response', commences within days after initial antigen encounter, unlike the secondary response that usually occurs weeks after priming. A further distinction of this response is that T-cell proliferation is driven by parenchymal cell antigen presentation, without requiring professional antigen presenting cells, but with increased dependence on IL-2. The mezzanine response might, therefore, be a new target for inhibiting T-cell responses in allograft rejection and autoimmunity or for enhancing T-cell responses in the context of microbial or tumour immunity.

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