A research team from Hokkaido University and Sapporo Medical University have studied the effect of the itaconate molecule on the immune system.
The researchers demonstrated that, in cell culture, ITA inhibited the differentiation of Th17 cells, which have the potential to develop autoimmune diseases, and promoted that of Treg cells, which can ameliorate them. Furthermore, in mouse models of experimental autoimmune encephalomyelitis, ITA reduced disease symptoms. Further testing was done to confirm that this effect was due to its effect on T cells.
Investigations into the mechanism of action of ITA revealed that it inhibits essential metabolic pathways, glycolysis, oxidative phosphorylation, and methionine metabolism in Th17 and Treg cells. The results explain the mechanisms underlying the modulation of T cell differentiation that could eventually lead to simple therapeutic approaches that regulate T cell differentiation, thus treating T cell-mediated autoimmune diseases.
These findings, which have implications for the treatment of autoimmune disorders, were published in the journal Nature Communications.