Social stressors associated with age-related T lymphocyte percentages in older US adults: Evidence from the Health and Retirement Study

Author:

Klopack Eric T.ORCID,Crimmins Eileen M.,Cole Steve W.,Seeman Teresa E.,Carroll Judith E.

Abstract

AbstractExposure to stress is a well-established risk factor of poor health and accelerated aging. Immune aging, including declines in naive and increases in late memory and terminally differentiated T cells, plays an important role in immune health and tissue specific aging, and may contribute to the observed elevated risk for poor health among those who experience high psychosocial stress. However, past data have been limited in estimating the contribution of life stress to the development of accelerated immune aging and investigating mediators such as lifestyle and CMV infection, that might be useful points of intervention. The current study utilizes a national sample of 5744 US adults over the age of 50 to assess the relationship of social stress (viz., everyday discrimination, stressful life events, lifetime discrimination, life trauma, and chronic stress) with flow cytometric estimates of immune aging, including naive and terminally differentiated T cell percentages and the ratio of CD4+ to CD8+ T cells. Experiencing life trauma and chronic stress was related to a lower percentage of CD4+ naive T cells. Higher everyday discrimination, lifetime discrimination, and chronic stress were each associated with a greater percentage of terminally differentiated CD4+ T cells. Stressful life events, high lifetime discrimination, and life trauma were related to a lower percentage of CD8+ naive T cells. Stressful life events, high lifetime discrimination and chronic stress were associated with a higher percentage terminally differentiated CD8+ T cells. High lifetime discrimination and chronic stress was related to a lower CD4+:CD8+ ratio. Lifestyle factors and cytomegalovirus (CMV) seropositivity partially reduced these effects. Results identify psychosocial stress as a contributor to accelerating immune aging by decreasing naive and increasing senescent T cells.

Publisher

Cold Spring Harbor Laboratory

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