Left: Depleting miR-342 from Tregs significantly worsened symptoms in the experimental autoimmune encephalitis (EAE) mouse model. Right: Overexpressing miR-342 in Tregs significantly improved EAE symptoms.

“Intronic miR342 is a master regulator of cellular glycolysis in Foxp3+ regulatory CD4 T cells.”

Rongzhen Yu, et al. – Northwestern University.

In this study, Yu and colleagues found that the microRNA miR-342 links metabolism and immune function in regulatory T cells (Tregs) in the experimental autoimmune encephalitis (EAE) mouse model of MS. Depleting miR-342 from Tregs exacerbated EAE symptoms, whereas overexpressing it in Tregs significantly reduced them. These changes are accompanied by shifts in Treg metabolism, with miR-342 depletion leading to the upregulation of every gene in the glycolysis pathway, and are specific to inflammatory contexts, as baseline levels of Tregs were unaltered in homeostatic conditions. These findings position miR-342, and Treg metabolism writ large, as a potential therapeutic target in MS.