Molecular mechanisms of aging control in the human immune system have been discovered

Based on multi-omic data (collected from different branches of science that study different levels of biological systems), the HIAC “immune clock” system allows you to assess the biological status of your body with an error of no more than 5.66 years. The model takes into account the proportions of cell subtypes (varieties of cells that differ in morphology, function, biochemical characteristics, or other features), specific changes in their transcriptomes (the complete set of mRNA molecules in a particular cell or tissue at a specific time), and the characteristics of T-cell receptors. Within this model, T-lymphocytes are recognized as the most sensitive indicators of aging. This approach allows for a shift from general population estimates to an individual analysis of each patient’s aging rate.

The individual rate of immune system aging directly correlates with the functional state of internal organs and overall metabolic health. Individuals with an immune age that is lower than their chronological age exhibit improved lung, liver, and blood glucose control. Their plasma contains higher concentrations of antioxidant and immunomodulatory molecules. This proves that the state of immunity serves as a primary marker of the overall biological wear and tear of the body, which manifests itself before the clinical symptoms of diseases.

At the molecular level, the RUNX1 factor plays a central role in maintaining the youthfulness of cells, and its concentration in T-lymphocytes progressively decreases over the years. The study revealed that the deficiency of this protein triggers the aging mechanism, leading to the shortening of telomeres and the loss of cell’s ability to divide effectively. A decrease in RUNX1 levels is closely associated with the accumulation of specific markers of cellular wear and tear, making this factor a biomarker of profound age-related changes in immune tissue.

Functional experiments have confirmed the possibility of reversing these processes by artificially restoring RUNX1 expression in old T cells. Increasing the level of this factor restores the cells’ protective functions, restores telomere length, and eliminates the signs of the age-related phenotype. The identification of RUNX1 as a functional brake on aging makes it the first confirmed internal target for therapeutic intervention. This discovery lays the foundation for the development of new immunotherapy methods aimed at prolonging active longevity and preventing age-related pathologies.