Cold exposure protects from neuroinflammation through immunologic reprogramming

This study shows that cold exposure reduces the symptoms of autoimmune disease by suppressing T cell activity through the modulation of monocytes. The study suggests that cold-induced metabolic adaptations may compete with autoimmunity as an energetic trade-off that can benefit immune-mediated diseases.

Scientific Research
Icetubs Manager


Maintaining a healthy immune system requires significant energy, which can be affected by environmental factors. Autoimmunity, which is a high-energy-demanding process, can compete with other biological programs, resulting in a milder immune response. This study investigated the effect of cold exposure on autoimmune disease and found that it reduced the immune response and attenuated multiple sclerosis in an animal model. This suggests that there is a competition between the thermogenic response to cold exposure and autoimmunity, which could have therapeutic implications for autoimmune-mediated or infectious diseases.


In conclusion, the impact of a metabolically active state on immunity and immune-mediated diseases is unclear, but recent research suggests that there may be a beneficial trade-off between cold-induced metabolic adaptations and autoimmunity. This is supported by the findings that cold exposure ameliorates active experimental autoimmune encephalomyelitis (EAE) by suppressing T cell priming and pathogenicity through the modulation of monocytes. The study provides a mechanistic link between environmental temperature and neuroinflammation, suggesting that competition between cold-induced metabolic adaptations and autoimmunity is energetically costly but beneficial for immune-mediated diseases. These findings may have important implications for the management of autoimmune diseases and highlight the need for further research in this area.

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