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    PTPN2 Deficiency Enhances Programmed T Cell Expansion and Survival Capacity of Activated T Cells

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    Author
    Flosbach, M; Oberle, SG; Scherer, S; Zecha, J; von Hoesslin, M; Wiede, F; Chennupati, V; Cullen, JG; List, M; Pauling, JK; ...
    Date
    2020-07-28
    Source Title
    Cell Reports
    Publisher
    CELL PRESS
    University of Melbourne Author/s
    Tiganis, Tony; Wiede, Florian
    Affiliation
    Sir Peter MacCallum Department of Oncology
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Flosbach, M., Oberle, S. G., Scherer, S., Zecha, J., von Hoesslin, M., Wiede, F., Chennupati, V., Cullen, J. G., List, M., Pauling, J. K., Baumbach, J., Kuster, B., Tiganis, T. & Zehn, D. (2020). PTPN2 Deficiency Enhances Programmed T Cell Expansion and Survival Capacity of Activated T Cells. CELL REPORTS, 32 (4), https://doi.org/10.1016/j.celrep.2020.107957.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/252499
    DOI
    10.1016/j.celrep.2020.107957
    Abstract
    Manipulating molecules that impact T cell receptor (TCR) or cytokine signaling, such as the protein tyrosine phosphatase non-receptor type 2 (PTPN2), has significant potential for advancing T cell-based immunotherapies. Nonetheless, it remains unclear how PTPN2 impacts the activation, survival, and memory formation of T cells. We find that PTPN2 deficiency renders cells in vivo and in vitro less dependent on survival-promoting cytokines, such as interleukin (IL)-2 and IL-15. Remarkably, briefly ex vivo-activated PTPN2-deficient T cells accumulate in 3- to 11-fold higher numbers following transfer into unmanipulated, antigen-free mice. Moreover, the absence of PTPN2 augments the survival of short-lived effector T cells and allows them to robustly re-expand upon secondary challenge. Importantly, we find no evidence for impaired effector function or memory formation. Mechanistically, PTPN2 deficiency causes broad changes in the expression and phosphorylation of T cell expansion and survival-associated proteins. Altogether, our data underline the therapeutic potential of targeting PTPN2 in T cell-based therapies to augment the number and survival capacity of antigen-specific T cells.

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