Protein kinase Cθ controls Th1 cells in experimental autoimmune encephalomyelitis

Shahram Salek-Ardakani, Takanori So, Beth S. Halteman, Amnon Altman, Michael Croft

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Abstract

Molecules that regulate encephalitogenic T cells are of interest for multiple sclerosis. In this study we show that protein kinase Cθ (PKCθ) is critical for the development of Ag-specific Th1 cells in experimental allergic encephalomyelitis (EAE), a model of multiple sclerosis. PKCθ-deficient mice immunized with myelin oligodendrocyte glycoprotein failed to develop cell infiltrates and Th1 cytokines in the CNS and were resistant to the development of clinical EAE. CD4 T cells became primed and accumulated in secondary lymphoid organs in the absence of PKCθ, but had severely diminished IFN-γ, TNF, and IL-17 production. Increasing Ag exposure and inflammatory conditions failed to induce EAE in PKCθ-deficient mice, showing a profound defect in the myelin oligodendrocyte glycoprotein-reactive T cell population. These data provide evidence of a pivotal role for PKCθ in the generation and effector function of autoimmune Th1 cells.

Original languageEnglish
Pages (from-to)7635-7641
Number of pages7
JournalJournal of Immunology
Volume175
Issue number11
Publication statusPublished - 2005 Dec 1

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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    Salek-Ardakani, S., So, T., Halteman, B. S., Altman, A., & Croft, M. (2005). Protein kinase Cθ controls Th1 cells in experimental autoimmune encephalomyelitis. Journal of Immunology, 175(11), 7635-7641.