期刊
出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.2202780119
关键词
socioeconomic status; immunosenescence; aging
资金
- USC/UCLA Center on Biodemography and Population Health through National Institute on Aging [P30AG017265]
- National Institute on Aging [NIA U01AG009740]
Exposure to stress is associated with accelerated immune aging, characterized by a decrease in naive T cells and an increase in terminally differentiated T cells.
Exposure to stress is a risk factor for poor health and accelerated aging. Immune aging, including declines in naive and increases in terminally differentiated T cells, plays a role in immune health and tissue specific aging, and may contribute to elevated risk for poor health among those who experience high psychosocial stress. 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 cytomegalovirus (CMV) infection. This study utilizes a national sample of 5,744 US adults over age 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(+) cells. Experiencing life trauma and chronic stress was related to a lower percentage of CD4(+) naive cells. Discrimination and chronic stress were each associated with a greater percentage of terminally differentiated CD4(+) cells. Stressful life events, high lifetime discrimination, and life trauma were related to a lower percentage of CD8(+) naive cells. Stressful life events, high lifetime discrimination, and chronic stress were associated with a higher percentage of terminally differentiated CD8(+) cells. High lifetime discrimination and chronic stress were related to a lower CD4(+):CD8(+) ratio. Lifestyle factors and CMV seropositivity partially reduced these effects. Results identify psychosocial stress as a contributor to accelerating immune aging by decreasing naive and increasing terminally differentiated T cells.
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