Chemical compounds from anthropogenic environment and immune evasion mechanisms: potential interactions

Julia Kravchenko, Emanuela Corsini, Marc A. Williams, William Decker, Masoud H. Manjili, Takemi Otsuki, Neetu Singh, Faha Al-Mulla, Rabeah Al-Temaimi, Amedeo Amedei, Anna Maria Colacci, Monica Vaccari, Chiara Mondello, A.Ivana Scovassi, Jayadev Raju, Roslida A. Hamid, Lorenzo Memeo, Stefano Forte, Rabindra Roy, Jordan Woodrick, Hosni K. Salem, Elizabeth P. Ryan, Dustin G. Brown, William H. Bisson, Leroy Lowe, H. Kim Lyerly

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.