Article
- The EMBO Journal (2004) 23, 1325 - 1335
- doi:10.1038/sj.emboj.7600133
Published online: 18 March 2004
Subject Category:
JunD regulates lymphocyte proliferation and T helper cell cytokine expression
Arabella Meixnera, Florian Karreth, Lukas Kenner and Erwin F Wagner
- Research Institute of Molecular Pathology (IMP), Vienna, Austria
Correspondence to:
Erwin F Wagner, Research Institute of Molecular Pathology (IMP), Dr Bohr-Gasse 7, A-1030 Vienna, Austria. Tel.: +43 1 797 30888; Fax: +43 1 798 9390; E-mail: wagner@imp.univie.ac.at
aPresent address: Institute of Molecular Biotechnology (IMBA), Dr Bohr-Gasse 3-5, A-1030 Vienna, Austria
Received 17 November 2003; Accepted 29 January 2004
Abstract
Transgenic mice broadly expressing JunD (Ubi-junDm) appear phenotypically normal, but have strongly reduced numbers of peripheral lymphocytes. JunD overexpression in lymphocytes does not protect from numerous apoptotic insults; however, transgenic T cells proliferate poorly and exhibit impaired activation due to reduced levels of IL-4, CD25 and CD69. Consistently, in the absence of JunD (junD-/-) T cells hyperproliferate following mitogen induction. Moreover, transgenic T helper (Th) 2 cells have decreased IL-4 and IL-10 expression, whereas junD-/- Th2 cells secrete higher amounts of both Th2 cytokines. Th1-polarized junD-/- CD4+ T cells display enhanced IFN-
cytokine production associated with upregulated T-bet expression and downregulated expression of suppressor of cytokine signaling-1. These novel findings demonstrate a regulatory role of JunD in T lymphocyte proliferation and Th cell differentiation.
Keywords:
- IL-4,
- IL-10,
- JunD,
- lymphocytes,
- SOCS1,
- T-bet,
- Th cells
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