IL-20 receptor 2 signaling down-regulates antigen-specific T cell responses

Christian Wahl, Werner Müller, Frank Leithäuser, Guido Adler, Franz Oswald, Jörg Reimann, Reinhold Schirmbeck, Anne Seier, Johannes Martin Weiss, Blair Prochnow, Ursula Maria Wegenka

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    The recently described cytokines IL-19, IL-20, and IL-24 share structural homology with IL-10 and are therefore classified as members of the IL-10 family of cytokines. Although it has long been speculated that signaling by their heterodimeric receptor complexes (IL-20R1/IL-20R2 and IL-22R/IL-20R2) influences immunological processes, the target cells for this group of cytokines are still unclear. By generating a knockout mouse strain deficient for the common IL-20R β-chain (IL-20R2), we show that IFN-γ and IL-2 secretion is significantly elevated after stimulation of IL-20R2-/--deficient CD8 and CD4 T cells with Con A or anti-CD3/CD28 in vitro. IL-10 secretion by activated IL-20R2-/- CD4 cells was diminished. Consistent with our in vitro results, significantly more Ag-specific CD8 IFN-γ+ and CD4 IFN-γ+ T cells developed to locally applied DNA vaccines in IL-20R2-deficient mice. In a T cell-dependent model of contact hypersensitivity, IL-20R2 knockout mice were more sensitive to the contact allergen trinitro-chloro-benzene. Thus, IL-20R2 signaling directly regulates CD8 and CD4 T cell answers in vitro and in vivo. For the first time, we provide evidence that IL-19, IL-20, and IL-24 are part of a signaling network that normally down-modulates T cell responses in mice. Copyright © 2009 by The American Association of Immunologists, Inc.
    Original languageEnglish
    Pages (from-to)802-810
    Number of pages8
    JournalJournal of Immunology
    Issue number2
    Publication statusPublished - 15 Jan 2009


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