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Significance Multiple sclerosis (MS) is a demyelinating disease of the CNS. Experimental autoimmune encephalomyelitis (EAE) is an animal model that has many similarities to MS. CNS-infiltrating, myelin-reactive T cells have pivotal roles in EAE/MS pathology, but the mechanisms governing pathogenic T cell function within the CNS remain poorly understood. Diacylglycerol O-acyltransferase-1 (DGAT1) is a normal lipid- and retinoid-metabolizing enzyme, but little is known about its role in T cells. We show that EAE is reduced in DGAT1-deficient mice. Moreover, our data suggest that T cell expression of DGAT1, by sequestering retinol, limits regulatory T cell (Treg) formation. Overall, our results implicate DGAT1 as a metabolic modulator of Treg induction, and add to the growing appreciation of the interplay between immunity and metabolism.

DGAT1 inhibits retinol-dependent regulatory T cell formation and mediates autoimmune encephalomyelitis