Social stress accelerates immune aging

Chronic exposure to stressful conditions is an established risk factor for poor health status, leading to faster and earlier development of age-related diseases and premature mortality. The literature highlights that the adverse effects of stress result from repeated and prolonged exposure to effects of the sympathoadrenal system. It increases inflammation, DNA damage, and telomere attrition, causing cellular damage. The outcome of these processes is cellular senescence. In addition, age-related changes in the immune system, leading to immunosenescence, contribute to systemic aging, organ failure, and premature mortality.

With aging, the immune cells' population composition shifts. In this context, the literature indicates a decrease in naïve (not exposed to antigen) B (produce antibodies) and T (recognize foreign antigens) cell pools coupled with an increase in terminally differentiated T cells pool. Also, there is an increase in CD8+ (cytotoxic T cells) cell supply relative to CD4+ (T-helper lymphocyte cells) T cells and an elevation in systemic inflammation. However, the rate at which these changes occur varies among individuals. This prompts further investigation to understand better why such variation exists. This is important because immune aging plays a role in multiple chronic conditions and the aging process itself.

To better characterize the reasons behind such variation, Klopack et al. focused on social stressors and challenges individuals face during adulthood. This is because social stress is believed to be a contributor to accelerated immune aging. The researchers chose to investigate five stress variables: stressful life events, chronic stress, everyday discrimination, lifetime discrimination, and life trauma. The sampled population included over 5,600 US adult participants over the age of 50.

Results revealed that exposure to more stressful events was associated with a lower proportion of naïve CD8+ and a higher percentage of terminally differentiated CD8+ cells. Also, greater chronic stress resulted in higher terminally differentiated CD4+ and CD8+ T cells and a lower proportion of CD4+ naïve T cells. With regard to experiencing everyday discrimination, it was associated with a higher percentage of terminally differentiated CD4+ cells. More significant lifetime discrimination resulted in a similar CD4+ and CD8+ T cells profile to chronic stress, except that the proportion of CD8+ naïve T cells was lower. Lastly, a higher number of life traumas resulted in a smaller percentage of naive CD+ and CD8+ T cells.

The authors concluded that psychosocial stress potentially contributes to accelerated immune aging. They prompted a further investigation to explore the potential of senolytic therapy in addressing issues associated with accelerated aging. Also, they recognized the importance of having interventions that reduce psychosocial stress and increase resilience.

Source: Klopack Eric T, Crimmins Eileen M, Cole Steve W, Seeman Teresa E, Carroll Judith E. Social stressors associated with age-related T lymphocyte percentages in older US adults: Evidence from the US Health and Retirement Study. Proceedings of the National Academy of Sciences. 2022;119(25):e2202780119.

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