Journal
JOURNAL OF IMMUNOLOGY
Volume 175, Issue 11, Pages 7635-7641Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.175.11.7635
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- NCI NIH HHS [CA91837] Funding Source: Medline
- NIAID NIH HHS [AI50498] Funding Source: Medline
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Molecules that regulate encephalitogenic T cells are of interest for multiple sclerosis. In this study we show that protein kinase CO (PKC theta) is critical for the development of Ag-specific Th1 cells in experimental allergic encephalomyelitis (EAE), a model of multiple sclerosis. PKC theta-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 PKC theta, but had severely diminished IFN-gamma, TNF, and IL-17 production. Increasing Ag exposure and inflammatory conditions failed to induce EAE in PKC theta-deficient mice, showing a profound defect in the myelin oligodendrocyte glycoprotein-reactive T cell population. These data provide evidence of a pivotal role for PKC theta in the generation and effector function of autoimmune Th1 cells.
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