Allison E Aiello1, Jennifer B Dowd2, Bamini Jayabalasingham3, Lydia Feinstein4, Monica Uddin5, Amanda M Simanek6, Caroline K Cheng7, Sandro Galea8, Derek E Wildman9, Karestan Koenen10, Graham Pawelec11. 1. Department of Epidemiology, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. Electronic address: aaiello@email.unc.edu. 2. CUNY School of Public Health, Hunter College, City University of New York, NY, USA. Electronic address: jdowd@hunter.cuny.edu. 3. CUNY School of Public Health, Hunter College, City University of New York, NY, USA. Electronic address: baminij@gmail.com. 4. Department of Epidemiology, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. Electronic address: lfeinst@email.unc.edu. 5. Department of Psychology, University of Illinois at Urbana-Champaign, Champaign, IL, USA. Electronic address: muddin@illinois.edu. 6. Joseph J. Zilber School of Public Health, University of Wisconsin-Milwaukee, Milwaukee, WI, USA. Electronic address: simaneka@uwm.edu. 7. School of Public Health, University of Michigan, Ann Arbor, MI, USA. Electronic address: kaiyi@med.umich.edu. 8. Boston University School of Public Health, Boston University, Boston, MA, USA. Electronic address: sgalea@bu.edu. 9. Department of Molecular and Integrative Physiology, University of Illinois at Urbana-Champaign, Urbana, IL, USA. Electronic address: wildmand@illinois.edu. 10. Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA, USA. Electronic address: kkoenen@hsph.harvard.edu. 11. Department of Internal Medicine II, Centre for Medical Research, University of Tubingen, Tubingen, Germany. Electronic address: graham.pawelec@uni-tuebingen.de.
Abstract
BACKGROUND: Psychosocial stress is thought to play a key role in the acceleration of immunological aging. This study investigated the relationship between lifetime and past-year history of post-traumatic stress disorder (PTSD) and the distribution of T cell phenotypes thought to be characteristic of immunological aging. METHODS: Data were from 85 individuals who participated in the community-based Detroit Neighborhood Health Study. Immune markers assessed included the CD4:CD8 ratio, the ratio of late-differentiated effector (CCR7-CD45RA+CD27-CD28-) to naïve (CCR7+CD45RA+CD27+CD28+) T cells, the percentage of KLRG1-expressing cells, and the percentage of CD57-expressing cells. RESULTS: In models adjusted for age, gender, race/ethnicity, education, smoking status, and medication use, we found that past-year PTSD was associated with statistically significant differences in the CD8+ T cell population, including a higher ratio of late-differentiated effector to naïve T cells, a higher percentage of KLRG1+ cells, and a higher percentage of CD57+ cells. The percentage of CD57+ cells in the CD4 subset was also significantly higher and the CD4:CD8 ratio significantly lower among individuals who had experienced past-year PTSD. Lifetime PTSD was also associated with differences in several parameters of immune aging. CONCLUSIONS: PTSD is associated with an aged immune phenotype and should be evaluated as a potential catalyzer of accelerated immunological aging in future studies.
BACKGROUND:Psychosocial stress is thought to play a key role in the acceleration of immunological aging. This study investigated the relationship between lifetime and past-year history of post-traumatic stress disorder (PTSD) and the distribution of T cell phenotypes thought to be characteristic of immunological aging. METHODS: Data were from 85 individuals who participated in the community-based Detroit Neighborhood Health Study. Immune markers assessed included the CD4:CD8 ratio, the ratio of late-differentiated effector (CCR7-CD45RA+CD27-CD28-) to naïve (CCR7+CD45RA+CD27+CD28+) T cells, the percentage of KLRG1-expressing cells, and the percentage of CD57-expressing cells. RESULTS: In models adjusted for age, gender, race/ethnicity, education, smoking status, and medication use, we found that past-year PTSD was associated with statistically significant differences in the CD8+ T cell population, including a higher ratio of late-differentiated effector to naïve T cells, a higher percentage of KLRG1+ cells, and a higher percentage of CD57+ cells. The percentage of CD57+ cells in the CD4 subset was also significantly higher and the CD4:CD8 ratio significantly lower among individuals who had experienced past-year PTSD. Lifetime PTSD was also associated with differences in several parameters of immune aging. CONCLUSIONS:PTSD is associated with an aged immune phenotype and should be evaluated as a potential catalyzer of accelerated immunological aging in future studies.
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