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PI3Kγ deficiency delays the onset of experimental autoimmune encephalomyelitis and ameliorates its clinical outcome.
Berod, Luciana Heinemann, Christina Heink, Sylvia Escher, Angelika Stadelmann, Christine Drube, Sebastian Wetzker, Reinhard Norgauer, Johannes Kamradt, Thomas
Berod, Luciana
Heinemann, Christina
Heink, Sylvia
Escher, Angelika
Stadelmann, Christine
Drube, Sebastian
Wetzker, Reinhard
Norgauer, Johannes
Kamradt, Thomas
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2011-03
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Abstract
PI3Ks control signal transduction triggered by growth factors and G-protein-coupled receptors and regulate an array of biological processes, including cellular proliferation, differentiation, survival and migration. Herein, we investigated the role of PI3Kγ in the pathogenesis of EAE. We show that, in the absence of PI3Kγ expression, clinical signs of EAE were delayed and mitigated. PI3Kγ-deficient myelin oligodendrocyte glycoprotein (MOG)(35-55) -specific CD4(+) T cells appeared later in the secondary lymphoid organs and in the CNS than their WT counterparts. Transfer of WT CD4(+) cells into PI3Kγ(-/-) mice prior to MOG(35-55) immunisation restored EAE severity to WT levels, supporting the relevance of PI3Kγ expression in Th cells for the pathogenesis of EAE; however, PI3Kγ was dispensable for Th1 and Th17 differentiation, thus excluding an altered expression of these pathogenetically relevant cytokines as the cause for ameliorated EAE in PI3Kγ(-/-) mice. These findings demonstrate that PI3Kγ contributes to the development of autoimmune CNS inflammation.
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PI3Kγ deficiency delays the onset of experimental autoimmune encephalomyelitis and ameliorates its clinical outcome. 2011, 41 (3):833-44 Eur. J. Immunol.
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en
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1521-4141