Cited by 76Toxic Organic Pollutants ImpactImmunotoxicology and immune responsesAir Quality and Health Impacts

The DOI matches its Crossref record; 34 of the 34 references it cites were found in a registry or an index.

Polycyclic aromatic hydrocarbons (PAHs) present in ambient urban dust drive proinflammatory T cell and dendritic cell responses via the aryl hydrocarbon receptor (AHR) in vitro

Open access

Abstract

Atmospheric particulate matter (PM) is a complex component of air pollution that is a composed of inorganic and organic constituents. The chemically-extracted organic fraction (OF) of PM excludes inorganics but retains most organic constituents like polycyclic aromatic hydrocarbons (PAHs). PAHs are ubiquitous environmental toxicants and known aryl hydrocarbon receptor (AHR) ligands. The AHR is a ligand activated transcription factor that responds to endogenous ligands and exogenous ligands including PAHs. Activation of the AHR leads to upregulation of cytochrome P450 (CYP) metabolizing enzymes which are important for the biotransformation of toxicants to less toxic, or in the case of PAHs, more toxic intermediates. Additionally, the AHR plays an important role in balancing regulatory and effector T cell responses. This study aimed to determine whether PAHs present in PM aggravate inflammation by driving inflammatory T cell and dendritic cell (DC) responses and their mechanism of action. This study tests the hypothesis that PAHs present in PM activate the AHR and alter the immune balance shifting from regulation to inflammation. To test this, the effects of SRM1649b OF on T cell differentiation and DC function were measured in vitro. SRM1649b OF enhanced Th17 differentiation in an AHR and CYP-dependent manner and increased the percent of IFNγ positive DCs in an AHR-dependent manner. SRM1649b PAH mixtures enhanced Th17 differentiation in an AHR-dependent but CYP-independent manner and increased the percent of IFNγ positive DCs. Cumulatively, these results suggest that PAHs present in PM are active components that contribute to immune responses in both T cells and BMDCs through the AHR and CYP metabolism. Understanding the role of AHR and CYP metabolism of PAHs in immune cells after PM exposure will shed light on new targets that will shift the immune balance from inflammation to regulation.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1371/journal.pone.0209690

Cites

34 of 34 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • PAHs can activate Toll-like receptors, activating intracellular pro-inflammatory pathways NF-κB and MAPK.

    “For instance, PAHs can activate Toll-like receptors (TLRs), activating intracellular pro-inflammatory pathways (nuclear factor-kappa B [NF-κB] and mitogen-activated protein kinase [MAPK])52.”

    From Air Pollution and Skin Diseases (2025) · cites this paper as [52]

    The Discussion reports that PAHs in particulate matter promote proinflammatory T-cell and dendritic-cell responses through AHR-related pathways. Our copy does not establish the claimed Toll-like receptor activation or downstream NF-κB and MAPK signaling (searched: Toll-like receptor, TLR, NF-κB, MAPK). (LLM, conf=0.82)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Metadata

Authors
O’Driscoll, C. A., Gallo, M. E., Hoffmann, E. J., Fechner, J. H., Schauer, J. J., Bradfield, C. A., & Mezrich, J. D.
Affiliations
University of Wisconsin–Madison (US)
Corresponding author
Mezrich, Joshua D.
Venue
PLOS ONE
Published
2018-12-21
Volume
13
Issue
12
Pages
e0209690
ISSN
1932-6203 (ISSN-L)
OpenAlex
W2906492750
Cited by
74
References
34
Citations by year
2026: 7 · 2025: 12 · 2024: 10 · 2023: 13 · 2022: 9 · 2021: 8 · 2020: 12 · 2019: 3
FWCI
2.84
Type
journal article
Language
en
Open access
Locations
  • PLoS ONE (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Figshare (submittedVersion, cc-by)
Funders
National Institute of Environmental Health Sciences (RO1 ES023842, R21 ES025304, T32 ES007015)
Topics
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Toxic Organic Pollutants Impact
  • Life Sciences › Immunology and Microbiology › Immunology › Immunotoxicology and immune responses
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Air Quality and Health Impacts
Keywords
polycyclic aromatic hydrocarbons, aryl hydrocarbon receptor, atmospheric particulate matter, urban dust, Th17 cell differentiation, dendritic cells, interferon-gamma, cytochrome P450 metabolism, T cell differentiation, regulatory T cells, environmental toxins
MeSH terms
Animals, Bone Marrow Cells, Cell Differentiation, Cytochromes, Dendritic Cells, Dust, Gene Expression Regulation, Humans, Lymphocyte Activation, Polycyclic Aromatic Hydrocarbons, T-Lymphocytes, Urban Health, Receptors, Aryl Hydrocarbon, Mice, Knockout, Cytochrome P-450 CYP1A1, Mice, Particulate Matter, Th17 Cells

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review