Discrimination and dendritic cell abundance among older adults in the health and retirement study

Abstract

We investigated whether peripheral blood dendritic cell (DC) abundance varies as a function of discrimination exposure in a national sample of older US adults (aged 50 + years) from the 2016 Venous Blood Study, a US Health and Retirement Study biomarker project. Density of myeloid DCs (mDC) and plasmacytoid DCs (pDC) were measured using multiparameter flow cytometry. Discrimination was assessed using the validated Everyday Discrimination Scale. Weighted linear regression models quantified associations between discrimination and natural-log transformed DC abundance, controlling for sociodemographic factors, chronic health conditions, and health behaviors. We tested whether these associations varied by race/ethnicity. For mDC, we found no significant overall association with discrimination. However, race/ethnicity significantly modified this relationship: among non-Hispanic White participants, a 1-SD increase in discrimination was associated with a non-significant 1.4 % increase in mDC count (p = 0.20), while non-Hispanic Black participants showed a significant 4.6 % decrease (interaction p = 0.021). For pDC, a 1-SD change in discrimination was significantly associated with a 2.4 % increase in abundance across all participants (95 % CI: 0.6 %, 4.3 %, p = 0.010), with no significant effect modification by race/ethnicity. In this nationally representative study of older Americans, discrimination exposure was associated with altered dendritic cell abundance, with distinct patterns by cell type and race/ethnicity. Increased pDC counts across all racial/ethnic groups suggest a common immunological response to discrimination, while divergent mDC responses between non-Hispanic Black and White participants indicate race-specific immune modulation. These findings reveal complex cellular pathways through which discrimination may differentially influence immune function and contribute to health inequities.

Keywords: Biological dysregulation; Biological stress; CTRA; Epigenetics; Internalizing; Lifestyle genomics; Middle-aged; Psychoneuroimmunology; Psychosocial stressors; Social genomics.