Scientists at the University of Geneva (UNIGE) showed that colder temperatures provoke a trade-off of energy resources between autoimmunity and thermogenesis in mice. Cold decreases the antigen-presenting protein—major histocompatibility complex class II (MHCII)—on monocytes at steady state and in various inflammatory conditions including in a mouse model of multiple sclerosis. In addition, cold suppresses T-cell priming and pathogenicity against the body’s own antigens through the modulation of monocytes, thereby reducing neuroinflammation in mouse models of multiple sclerosis.