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    Mesoangioblasts Suppress T Cell Proliferation Through IDO and PGE-2-Dependent Pathways


    English, Karen and Tonlorenzi, Rossana and Cossu, Giulio and Wood, Kathryn J (2013) Mesoangioblasts Suppress T Cell Proliferation Through IDO and PGE-2-Dependent Pathways. Stem Cells and Development, 22 (3). pp. 512-523. ISSN 1547-3287

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    Abstract

    Human mesoangioblasts are vessel-associated stem cells that are currently in phase I/II clinical trials for the treatment of patients with Duchenne muscular dystrophy. To date, little is known about the effect of mesoangioblasts on human immune cells and vice versa. We hypothesized that mesoangioblasts could modulate the function of immune cells in a similar manner to mesenchymal stromal cells. Human mesoangioblasts did not evoke, but rather potently suppressed human T-cell proliferation and effector function in vitro in a dose- and timedependent manner. Furthermore, mesoangioblasts exert these inhibitory effects uniformly on human CD4+ and CD8+ T cells in a reversible manner without inducing a state of anergy. Interferon (IFN)-g and tumor necrosis factor (TNF)-a play crucial roles in the initial activation of mesoangioblasts. Indoleamine 2,3-dioxygenase (IDO) and prostaglandin E-2 (PGE) were identified as key mechanisms of action involved in the mesoangioblast suppression of T-cell proliferation. Together, these data demonstrate a previously unrecognized capacity of mesoangioblasts to modulate immune responses.

    Item Type: Article
    Keywords: Mesoangioblasts Suppress T Cell Proliferation; IDO; PGE-2-Dependent Pathways;
    Academic Unit: Faculty of Science and Engineering > Biology
    Item ID: 6844
    Identification Number: https://doi.org/10.1089/scd.2012.0386
    Depositing User: Karen English
    Date Deposited: 19 Jan 2016 16:45
    Journal or Publication Title: Stem Cells and Development
    Publisher: Mary Ann Liebert
    Refereed: Yes
    URI:
    Use Licence: This item is available under a Creative Commons Attribution Non Commercial Share Alike Licence (CC BY-NC-SA). Details of this licence are available here

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