Cold exposure protects against neuroinflammation through immunological reprogramming

Open Access Publication Date: October 22, 2021 DOI: https : //doi.org/10.1016/j.cmet.2021.10.002

Description

Autoimmunity is energetically costly, and the effects of a metabolically active state on immunity and immune disease are unknown.

Ly6C monocytes are important effectors of CNS autoimmunity and have been implicated in an elusive role in priming naive autoreactive T cells.

Here, we analyzed immune changes in different compartments during cold exposure and showed that energetically expensive stimulation markedly ameliorates active experimental autoimmune encephalomyelitis (EAE).

Cold exposure reduces monocyte MHCII in steady state and in various inflammatory mouse models, and suppresses T cell priming and virulence through monocyte regulation.

Genetic and antibody-mediated depletion of monocytes and adoptive transfer of Th1 or Th17 polar cells to EAE nullify the cold-induced effects on T cells or EAE, respectively.

The results are based on animal experiments and should be interpreted with caution.