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Updated: Apr 12, 2026

Immunometabolic Circuits in Infection for Advancing Host Directed Therapies
Published on: September 13, 2024
Chemical compounds from anthropogenic environment and immune evasion mechanisms: potential interactions
Julia Kravchenko1, Emanuela Corsini2, Marc A Williams3
1Department of Surgery, Duke University Medical Center, Durham, NC 27710, USA; julia.krauchanka@duke.edu.
Abstract:
An increasing number of studies suggest an important role of host immunity as a barrier to tumor formation and progression. Complex mechanisms and multiple pathways are involved in evading innate and adaptive immune responses, with a broad spectrum of chemicals displaying the potential to adversely influence immunosurveillance. The evaluation of the cumulative effects of low-dose exposures from the occupational and natural environment, especially if multiple chemicals target the same gene(s) or pathway(s), is a challenge. We reviewed common environmental chemicals and discussed their potential effects on immunosurveillance. Our overarching objective was to review related signaling pathways influencing immune surveillance such as the pathways involving PI3K/Akt, chemokines, TGF-β, FAK, IGF-1, HIF-1α, IL-6, IL-1α, CTLA-4 and PD-1/PDL-1 could individually or collectively impact immunosurveillance. A number of chemicals that are common in the anthropogenic environment such as fungicides (maneb, fluoxastrobin and pyroclostrobin), herbicides (atrazine), insecticides (pyridaben and azamethiphos), the components of personal care products (triclosan and bisphenol A) and diethylhexylphthalate with pathways critical to tumor immunosurveillance. At this time, these chemicals are not recognized as human carcinogens; however, it is known that they these chemicalscan simultaneously persist in the environment and appear to have some potential interfere with the host immune response, therefore potentially contributing to promotion interacting with of immune evasion mechanisms, and promoting subsequent tumor growth and progression.
Insights
Common environmental chemicals can disrupt immune surveillance, potentially promoting tumor growth. Evaluating cumulative low-dose exposures is crucial for understanding cancer risk and immune evasion mechanisms.
Area of Science:
- Environmental toxicology
- Immunology
- Cancer research
Background:
- Host immunity is a critical barrier against tumor formation and progression.
- Environmental chemicals can interfere with innate and adaptive immune responses, impacting immunosurveillance.
- Cumulative effects of low-dose, multi-chemical exposures pose a significant challenge in risk assessment.
Purpose of the Study:
- To review common environmental chemicals and their potential effects on immunosurveillance.
- To discuss signaling pathways critical to tumor immunosurveillance that may be influenced by these chemicals.
- To highlight the potential role of environmental chemicals in promoting tumor immune evasion.
Main Methods:
- Literature review of common environmental chemicals and their impact on immune surveillance pathways.
- Analysis of signaling pathways including PI3K/Akt, chemokines, TGF-β, FAK, IGF-1, HIF-1α, IL-6, IL-1α, CTLA-4, and PD-1/PDL-1.
- Identification of specific chemicals such as fungicides, herbicides, insecticides, and personal care product components.
Main Results:
- Several common environmental chemicals (e.g., fungicides, herbicides, triclosan, BPA) can interfere with critical immune surveillance pathways.
- These chemicals, though not classified as carcinogens, can collectively impact host immune response and promote immune evasion.
- The review identified specific chemicals and their potential to interact with pathways crucial for tumor immunosurveillance.
Conclusions:
- Environmental chemicals can subvert tumor immunosurveillance, potentially contributing to cancer progression.
- Understanding the impact of these chemicals on immune evasion mechanisms is essential for assessing cancer risk.
- Further research is needed to evaluate the cumulative effects of low-dose environmental chemical exposures on cancer development.
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