A new study sheds light on why as people age they become more susceptible to cold. According to researchers at Yale and the University of California-San Francisco, the culprit is the same immune cells within fat that are designed to protect us from cold temperatures.

In the study published today in Cell Metabolism, the team found that the fat tissue of older mice loses the immune cell group 2 innate lymphoid cells (ILC2), which restore body heat in the presence of cold temperatures. But they also found that stimulating production of new ILC2 cells in aging mice actually makes them more prone to cold-induced death.

Vishwa Deep Dixit, co-corresponding author of the study, and his colleagues were curious about why fat tissue harbors immune system cells. When they sequenced genes from cells of old and young mice, they found that older animals lacked ILC2 cells, a deficit that limited their ability to burn fat and raise their body temperature in cold conditions.

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When they introduced a molecule that boosts the production of ILC2 in aging mice, the immune system cells were restored but the mice were surprisingly even less tolerant of cold temperatures.

“The simple assumption is that if we restore something that is lost, then we are also going to restore life back to normal,” Dixit said. “But that is not what happened. Instead of expanding healthy cells of youth, the growth factor ended up multiplying the bad ILC2 cells that remained in fat of old mice.”

But when researchers took ILC2 cells from younger mice and transplanted them into older mice, they found, the older animals’ ability to tolerate cold was restored.

“Immune cells play a role beyond just pathogen defense and help maintain normal metabolic functions of life,” Dixit said. “With age, the immune system has already changed and we need to be careful how we manipulate it to restore the health of elderly.”