Modulation of cancer immunosurveillance by infections: a particular hygiene hypothesis for tumor growth ?
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Abstract
Abstract
Cancer results from a multi-step biological process consecutive to uncontrolled replication of transformed cells in which interactions with the surrounding environment and the host immune system play a major role. Anti-tumoral immune responses, mediated mostly by cytotoxic T cells, natural killer cells, and NK/T cells are in charge for killing the malignant cells and eradicating the tumor. At the early stages of cancer development they usually provide the appropriate immunosurveillance that eliminates most of the transformed cells.
The connection between cancers and infections, mostly by viruses, has attracted major attention. Roughly 12% of all human cancers are caused by oncoviruses via complex mechanisms involving host genetic variability and viral oncogenesis, while, in contrast, oncolytic viruses selectively infect and kill malignant cells. In addition to these direct effects of viruses on tumor cells, infections by viruses as well as by other agents, as key activators of the immune system, may enhance the efficacy of cancer immunosurveillance through bystander modulation.
This review provides an overview of the concept of immunosurveillance with highlighting its main cellular arms. We discuss the role of infections on cancer development and especially evidences of a positive effect of infections on the inhibition of some cancer development through enhancement of innate immune responses. This effect of infection might constitute a peculiar type of hygiene hypothesis, which could lead to distinct frequency of some cancers in populations with different exposure to infectious agents.
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