Older mammals are prone to impaired thermoregulation, such as the inability to generate sufficient warmth in response to cold temperature. Researchers here find that changes in the population of ICL2 immune cells in fat tissue are important in this dysfunction. Transplanting young immune cells into old mice appears to help, but that demonstration is just the starting point. Researchers will now have to work their way down the long road to a sufficient understanding of the underlying mechanisms to enable a cost-effective forms of intervention. How does this dysfunction connect to the underlying cell and tissue damage of aging? That question will likely remain open for some years.
Human evolution has provided us a level of protection from the existential threat of cold temperature with the capacity to produce heat from fat stored in the body. However, with age, people become more susceptible to cold as well as inflammation and metabolic problems which can lead to a host of chronic diseases. In a new study, researchers find that the fat tissue of older mice loses the immune cell group 2 innate lymphoid cells (ILC2) which restore body heat in presence of cold temperatures. But in a cautionary tale for those seeking easy treatments for diseases of aging, they also found that stimulating production of new ILC2 cells in aging mice actually makes them more prone to cold-induced death.
Researchers were curious about why fat tissue harbors immune system cells, which are usually concentrated in areas often exposed to pathogens like nasal passages, lungs, and skin. When they sequenced genes from cells of old and young mice they found that older animals lacked ILC2 cells, a deficit which limited their ability to burn fat and raise their body temperature in cold conditions. When scientists introduced a growth factor 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. 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 that the older animals' ability to tolerate cold was restored.