# Discovery of Blood-Based Proteins That Mark Benzo[a]pyrene Modulation of Autoimmunity

**Authors:** Kameron Kennicott, Yilin Nie, Yun Liang

PMC · DOI: 10.3390/ijms262010242 · International Journal of Molecular Sciences · 2025-10-21

## TL;DR

The study identifies blood proteins affected by benzo[a]pyrene exposure, which could help detect early immune changes linked to autoimmune diseases.

## Contribution

The study discovers blood-based proteins modulated by BaP that precede autoimmune symptoms and may serve as biomarkers.

## Key findings

- BaP exposure upregulates cytokines like IL1a and IFNg months before autoimmune symptoms appear.
- Proteins such as IL16, IL22, and SNCA are elevated in male MRL mice, potentially linking to autoimmune damage.
- Blood and peripheral organ immune responses to BaP show distinct patterns.

## Abstract

Environmental pollutants are thought to shape our immune landscape and drive the rise in autoimmune disease incidence worldwide. However, the molecular underpinnings of environmental impact on autoimmunity remain elusive and a quantitative measurement for immune dysfunction as a result of environmental exposure is yet to be developed. To this end, we have performed a discovery study to identify blood-based, immune-associated proteins regulated by benzo[a]pyrene (BaP) using the autoimmune-prone murine model MRL. We report the upregulation of autoimmune-associated cytokines including IL1a and IFNg by BaP, months before the manifestation of autoimmune phenotypes. Additionally, the increased levels of proteins such as IL16, IL22 and SNCA in male MRL mice upon BaP exposure may be a molecular link to the increased risk in end organ damage in subsets of autoimmune disease patients. Further comparison with the transcriptomic analysis of BaP-stimulated skin and lungs suggests distinct patterns of immune regulation in peripheral organs versus blood. Altogether, our study supports the need for the early detection of BaP-induced immune changes for the prevention and management of autoimmune diseases and provides leads for the future development of these blood-based biomarkers.

## Linked entities

- **Proteins:** IL1A (interleukin 1 alpha), IFNG (interferon gamma), IL16 (interleukin 16), IL22 (interleukin 22), SNCA (synuclein alpha)
- **Chemicals:** benzo[a]pyrene (PubChem CID 2336), BaP (PubChem CID 2336)
- **Diseases:** autoimmune disease (MONDO:0007179)

## Full-text entities

- **Genes:** Ifng (interferon gamma) [NCBI Gene 15978] {aka IFN-g, If2f, Ifg}, Il16 (interleukin 16) [NCBI Gene 16170] {aka mKIAA4048}, Il22 (interleukin 22) [NCBI Gene 50929] {aka IL-22, IL-22a, ILTIFa, If2b1, Iltif}, Snca (synuclein, alpha) [NCBI Gene 20617] {aka NACP, alpha-Syn, alphaSYN}, Il1a (interleukin 1 alpha) [NCBI Gene 16175] {aka Il-1a}
- **Diseases:** autoimmune (MESH:D001327), immune dysfunction (MESH:D007154), end organ damage (MESH:C564816)
- **Chemicals:** BaP (MESH:D001564)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12565278/full.md

## References

95 references — full list in the complete paper: https://tomesphere.com/paper/PMC12565278/full.md

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Source: https://tomesphere.com/paper/PMC12565278