Citation
Kravchenko, Julia and Corsini, Emanuela and Williams, Marc A. and Decker, William and Manjili, Masoud H. and Otsuki, Takemi and Singh, Neetu and Al-Mulla, Faha and Al-Temaimi, Rabeah and Amedei, Amedeo and Colacci, Anna Maria and Vaccari, Monica and Mondello, Chiara and Scovassi, A. Ivana and Raju, Jayadev and A. Hamid, Roslida and Memeo, Lorenzo and Forte, Stefano and Roy, Rabindra and Woodrick, Jordan and Salem, Hosni K.
(2015)
Chemical compounds from anthropogenic environment and immune evasion mechanisms: potential interactions.
Carcinogenesis, 36 (suppl. 1).
pp. 111-127.
ISSN 0143-3334; ESSN: 1460-2180
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.
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