Leonard Davis School of Gerontology, University of Southern California, Los Angeles, CA 90089.
Cousins Center for Psychoneuroimmunology, Jane & Terry Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, CA 90095.
Proc Natl Acad Sci U S A. 2022 Jun 21;119(25):e2202780119. doi: 10.1073/pnas.2202780119. Epub 2022 Jun 13.
Exposure to stress is a risk factor for poor health and accelerated aging. Immune aging, including declines in naïve 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 naïve 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 naïve 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 naïve 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 naïve and increasing terminally differentiated T cells.
暴露于压力是健康状况不佳和加速衰老的一个风险因素。免疫衰老,包括幼稚 T 细胞的减少和终末分化 T 细胞的增加,在免疫健康和组织特异性衰老中起作用,并且可能导致经历高心理社会压力的人健康状况不佳的风险增加。过去的数据在估计生活压力对加速免疫衰老的发展的贡献以及研究生活方式和巨细胞病毒 (CMV) 感染等介质方面受到限制。本研究利用 5744 名 50 岁以上美国成年人的全国样本,评估社会压力(即日常歧视、生活压力事件、终生歧视、生活创伤和慢性压力)与流式细胞术估计的免疫衰老之间的关系,包括幼稚和终末分化 T 细胞的百分比以及 CD4 与 CD8 细胞的比值。经历生活创伤和慢性压力与 CD4 幼稚细胞的百分比较低有关。歧视和慢性压力均与更多的终末分化 CD4 细胞百分比有关。生活压力事件、高终生歧视和生活创伤与 CD8 幼稚细胞的百分比较低有关。生活压力事件、高终生歧视和慢性压力与终末分化 CD8 细胞的百分比较高有关。高终生歧视和慢性压力与 CD4:CD8 比值较低有关。生活方式因素和 CMV 血清阳性率部分降低了这些影响。结果表明,心理社会压力通过减少幼稚 T 细胞和增加终末分化 T 细胞而加速免疫衰老。