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    Marek's disease virus modulates T cell proliferation via activation of cyclooxygenase 2-dependent prostaglandin E2 (2021)

    Art
    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Autoren
    Kamble, Nitin
    Gurung, Angila
    Kaufer, Benedikt B. (WE 5)
    Pathan, Ansar Ahmed
    Behboudi, Shahriar
    Quelle
    Frontiers in immunology
    Bandzählung: 12
    Seiten: Article 801781
    ISSN: 1664-3224
    Sprache
    Englisch
    Verweise
    URL (Volltext): https://www.frontiersin.org/articles/10.3389/fimmu.2021.801781/full
    DOI: 10.3389/fimmu.2021.801781
    Pubmed: 35003129
    Kontakt
    Institut für Virologie

    Robert-von-Ostertag-Str. 7-13
    14163 Berlin
    +49 30 838 51833
    virologie@vetmed.fu-berlin.de

    Abstract / Zusammenfassung

    Marek's disease virus (MDV), an avian alphaherpesvirus, infects chickens, transforms CD4+ T cells, and induces immunosuppression early during infection. However, the exact mechanisms involved in MDV-induced immunosuppression are yet to be identified. Here, our results demonstrate that MDV infection in vitro and in vivo induces activation of cyclooxygenase-2 (COX-2) and production of prostaglandin E2 (PGE2). This exerts its inhibitory effects on T cell proliferation at day 21 post infection via PGE2 receptor 2 (EP2) and receptor 4 (EP4). Impairment of the MDV-induced T cell proliferation was associated with downregulation of IL-2 and transferrin uptake in a COX-2/PGE2 dependent manner in vitro. Interestingly, oral administration of a COX-2 inhibitor, meloxicam, during MDV infection inhibited COX-2 activation and rescued T cell proliferation at day 21 post infection. Taken together, our results reveal a novel mechanism that contributes to immunosuppression in the MDV-infected chickens.