Multiple sclerosis is characterized by the destruction of oligodendrocytes and myelin sheath in the central nervous system (CNS). Curcumin inhibits experimental allergic encephalomyelitis (EAE), a model for multiple sclerosis, by blocking IL-12 signaling in T cells, suggesting that it would be effective in the treatment of multiple sclerosis. Natarajan and Bright investigated the effect of curcumin on the pathogenesis of CNS demyelination in EAE . In vivo treatment of SJL/J mice with curcumin significantly reduced the duration and clinical severity of active immunization and adoptive transfer in EAE . Curcumin inhibited EAE in association with a decrease in IL-12 production from macrophage/microglial cells and differentiation of neural antigen-specific Th1 cells. In vitro treatment of activated T cells with curcumin inhibited IL-12-induced tyrosine phosphorylation of Janus kinase 2, tyrosine kinase 2, and STAT3 and STAT4 transcription factors. Inhibition of the Janus kinase-STAT pathway by curcumin resulted in a decrease in IL-12-induced T-cell proliferation and Th1 differentiation. These findings show that curcumin inhibits EAE by blocking IL-12 signaling in T cells and suggest a rationale for its use in the treatment of multiple sclerosis and other Th1 cell-mediated inflammatory diseases.
Verbeek and coworkers examined the effects of curcumin on autoimmune T-cell reactivity in mice and on the course of EAE. Continuous oral administration of curcumin significantly affected antigen-specific proliferation and interferon-gamma production by lymph node-derived T cells following immunization with an EAE-inducing peptide . The overall effects of oral curcumin were mild but beneficial.
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