# Social disadvantage and immune gene expression in an urban US population

> **NIH NIH F32** · DUKE UNIVERSITY · 2022 · $67,582

## Abstract

PROJECT SUMMARY
 Social adversity is one of the most robust predictors of poor health, increased disease susceptibility, and
shorter lifespan in the United States. Recent work in experimental animal models suggests that these
relationships cannot be fully explained by health risk behaviors or health selection, and that changes in immune
gene regulation also play a role. Intriguingly, many of the biological pathways affected by social adversity in
animal models are also correlated with social adversity in humans. To date, however, most studies in humans
have focused on clinical or opportunistically collected samples, and none have yet investigated how social
disadvantage influences the gene expression response to environmental challenges, such as pathogen infection,
that may further amplify social environmental effects.
 The goal of the proposed research is to address these gaps by taking advantage of a unique population-
representative sample of Detroit, collected by the Detroit Neighborhood Health Study (DNHS). The DNHS
combines extensive neighborhood and individual-level data on social disadvantage with genotype data and,
crucially, a biobank of cryopreserved peripheral blood mononuclear cells (PBMCs) from the same study subjects.
I will use this resources to address three questions. First, what effect does social disadvantage, across multiple
measures, have on baseline immune gene expression in humans? This aim will extend studies of social adversity
and immune gene expression to an urban American population in which the relative impact of multiple types of
social adversity (e.g., low socioeconomic status, recent trauma, neighborhood-level poverty) can be assessed.
Second, to what degree does genotype moderate the effect of social environment on immune gene regulation?
This analysis will highlight whether genetic differences are important in shaping susceptibility to social adversity,
using immune gene expression as a model. Third, to what degree does social disadvantage affect the immune
response to viral challenges (cytomegalovirus and Epstein-Barr virus) which have been shown to follow a social
gradient in this population? This analysis will provide insight into whether social disadvantage-associated
differences in immune function contribute to social gradients in viral infection by assessing the gene expression
response to ex vivo viral challenge, in primary PBMCs collected from DNHS study subjects.
 These analyses will provide insight into the role of social adversity in shaping immune function across the
spectrum of social disadvantage in the US. The proposed work will both add to the growing literature on social
adversity and gene expression in humans, and shed light on the role of genotype and pathogen environment in
creating heterogeneity in this relationship. It will also introduce two powerful methods from functional and
statistical genomics (expression quantitative trait locus mapping and ex vivo challenges in cell culture) to the
...

## Key facts

- **NIH application ID:** 10292912
- **Project number:** 5F32AG067704-02
- **Recipient organization:** DUKE UNIVERSITY
- **Principal Investigator:** Christopher Ryan Campbell
- **Activity code:** F32 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $67,582
- **Award type:** 5
- **Project period:** 2020-12-01 → 2023-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10292912

## Citation

> US National Institutes of Health, RePORTER application 10292912, Social disadvantage and immune gene expression in an urban US population (5F32AG067704-02). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/10292912. Licensed CC0.

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