Researchers at RIKEN have discovered that the absence of a critical signaling molecule in specific immune cells can trigger a range of age-related illnesses in young mice. This significant finding has the potential to contribute to the development of novel therapies for age-related illnesses.

Aging affects the immune system negatively

Aging has negative effects on the immune system, leading to a condition called inflammation. Inflammaging is characterized by chronic, low-grade inflammation, even in the absence of pathogens. This inflammation damages tissues and makes older individuals more vulnerable to infections, as well as diseases like type II diabetes, heart disease, and cancer.

Inflammaging also triggers T cells, immune cells responsible for recognizing and responding to pathogens, to become overactive and produce inflammation-causing substances called chemokines and cytokines. This state of T cell overdrive is known as senescence.

According to Takashi Saito from the RIKEN Center for Integrative Medical Sciences, there is a common misconception that aging leads to reduced cell activity. However, certain aged immune cells can become activated, resulting in inflammation. The receptor-interacting protein kinase 1 (RIPK1), a signaling molecule, plays a role in cell death through different pathways based on its interactions with other compounds. Recent research suggests that individuals with a deficiency in RIPK1 may have an increased vulnerability to inflammatory disorders.

The absence of RIP1 protein in T cells results in inflammatory diseases

The study published in the journal Science Advances reveals that the absence of a protein called RIPK1 in T cells of mice leads to the development of inflammatory diseases at a young age and premature death. The T cells lacking RIPK1 exhibit similar behavior to T cells in aged mice, suggesting a connection between RIPK1 and aging.

Researchers discovered that without RIPK1, caspase-8 and RIPK3 compounds excessively activate a cell-growth regulator called mTORC1, leading to T-cell senescence. This activation induces the expression of genes associated with cellular aging, resulting in the production of various chemokines and cytokines.

A notable observation was that senescent T cells placed in normal mice returned to a non-senescent state, suggesting that environmental factors are influential in regulating T cell senescence.