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    PIM-2 protein kinase negatively regulates T cell responses in transplantation and tumor immunity

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    95407.2-20180620170110-covered ...
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    Author
    Daenthanasanmak, Anusara
    Wu, Yongxia
    Iamsawat, Supinya
    Nguyen, Hung D.
    Bastian, David
    Zhang, MengMeng
    Sofi, M. Hanief
    Chatterjee, Shilpak
    Hill, Elizabeth G.
    Mehrotra, Shikhar
    Kraft, Andrew S.
    Yu, Xue-Zhong
    Show allShow less
    Affiliation
    Univ Arizona, Ctr Canc
    Issue Date
    2018-07-02
    
    Metadata
    Show full item record
    Publisher
    AMER SOC CLINICAL INVESTIGATION INC
    Citation
    J Clin Invest. 2018;128(7):2787-2801. https://doi.org/10.1172/JCI95407.
    Journal
    JOURNAL OF CLINICAL INVESTIGATION
    Rights
    Copyright © 2018, American Society for Clinical Investigation
    Collection Information
    This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.
    Abstract
    PIM kinase family members play a crucial role in promoting cell survival and proliferation via phosphorylation of their target substrates. In this study, we investigated the role of the PIM kinases with respect to T cell responses in transplantation and tumor immunity. We found that the PIM-2 isoform negatively regulated T cell responses to alloantigen, in contrast to the PIM-1 and PIM-3 isoforms, which acted as positive regulators. T cells deficient in PIM-2 demonstrated increased T cell differentiation toward Th1 subset, proliferation, and migration to target organs after allogeneic bone marrow transplantation, resulting in dramatically accelerated graft-versus-host disease (GVHD) severity. Restoration of PIM-2 expression markedly attenuated the pathogenicity of PIM-2-deficient T cells to induce GVHD. On the other hand, mice deficient in PIM-2 readily rejected syngeneic tumor, which was primarily dependent on CD8(+) T cells. Furthermore, silencing PIM-2 in polyclonal or antigen-specific CD8(+) T cells substantially enhanced their antitumor response in adoptive T cell immunotherapy. We conclude that PIM-2 kinase plays a prominent role in suppressing T cell responses, and provide a strong rationale to target PIM-2 for cancer immunotherapy.
    ISSN
    0021-9738
    1558-8238
    PubMed ID
    29781812
    DOI
    10.1172/JCI95407
    10.1172/JCI95407DS1
    Version
    Final published version
    Sponsors
    Biostatistics Shared Resource, Hollings Cancer Center, Medical University of South Carolina [P30 CA138313]; University of Arizona Cancer Center [P30 CA023074]; NIH [R01CA173200, R01 CA169116, R01 AI118305, R01 HL137373, R21 CA192202]; DOD [W81XWH-12-1-0560]; SmartState Endowment in Cancer Stem Cell Biology & Therapy Program
    Additional Links
    https://www.jci.org/articles/view/95407
    http://www.jci.org/articles/view/95407/sd/1
    ae974a485f413a2113503eed53cd6c53
    10.1172/JCI95407
    Scopus Count
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    UA Faculty Publications

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