Lately, the article “Cxxc finger protein 1 maintains homeostasis and function of intestinal group 3 innate lymphoid cells with aging” was published by team of Lie Wang from the Future Health Laboratory of Innovation Center of Yangtze River Delta, team of Han Laing from MD Anderson Cancer Center, and team of Chuan Wu from National Cancer Institute.

The study found that homeostatic decline of ILC3s is mainly manifested by a decrease in CCR6+ ILC3 subsets, especially a decrease in CCR6+CD4+ ILC3s and an increase in NKp46+ ILC3s for aged mice. Homeostatic decline of ILC3s is companied by functional decline for aged mice, and a reduction in secretion of IL-22 and IL-17A restrict host’s capability of resistance to infection. Homeostatic maintenance of CCR6+ ILC3s is regulated by endogenous protective mechanisms while NKp46+ ILC3 is more affected by intestinal microenvironment and metabolic changes. In addition, the experimental data of this study reflects the impact of epigenetic regulation on homeostasis of innate lymphoid cells in aging, and indicates that ILC3s in the targeting intestine may be new breakthroughs for improving age-related infection.

In recent years, population aging has been more severe. The regression of immunologic function will result in poor vaccination responses, persistent low-grade inflammation and increased infection susceptibility with aging. As a complex organ system with multiple immune cell types, the intestine shows homeostatic dysregulation and functional decline with aging. ILC3s maintain the epithelial barrier integrity by producing interleukin -22 and interleukin -17A, they also participate in adjusting the initiation and immunologic tolerance of regulatory cells (Tregs), which tightly related to intestinal dynamic equilibrium. Therefore, exploring homeostatic and functional changes of ILC3s is of great significance for improving health at the old age.