Abstract
Abstract Recent studies have shown that diferuloylmethane (curcumin) ameliorates autoimmune diseases, including multiple sclerosis, rheumatoid arthritis, lupus and diabetes in animal and human models. We examined the effects of curcumin and its metabolites on the immune response in NOD mice. We assessed their ability to regulate pro-inflammatory cytokines and the differentiation of IFNγ-producing T cells. We also determined whether curcumin could affect Treg development and production of the anti-inflammatory cytokine, IL-10. NOD dendritic cells (DC) treated with curcumin in vitro produce decreased pro-inflammatory cytokines, including IL-12. Treatment of DC with ferulic acid and vanillin, two metabolites of curcumin, also downregulated production of IL-12. This effect was not due to an decrease in DC viability or increased production of IL-10. More importantly, NOD DC treated with curcumin and its metabolites induce fewer IFNγ-producing T cells, shown to be responsible for beta islet destruction. Mice treated with curcumin were protected from disease and this protection was associated with a decrease in IFNγ production in the spleen and pancreatic LN. Although CD103+ DC harvested from the mesenteric LN of curcumin-treated NOD mice were better at inducing in vitro Treg conversion, the levels of CD4+Foxp3+ and CD4+Foxp3+Neuropilin- cells in the pancreatic LN were actually impaired in those mice. Overall, our in vitro and in vivo data show that curcumin and its metabolites suppress the differentiation of IFNg-producing cells involved in type 1 diabetes development. Curcumin or its metabolites may have therapeutic potential for the prevention of type 1 diabetes.
Published Version
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