Immune effectors responsible for the elimination of hyperploid cancer cells

Oncoimmunology
Fernando ArandaLaura Senovilla

Abstract

The immune system avoids oncogenesis and slows down tumor progression through a mechanism called immunosurveillance. Nevertheless, some malignant cells manage to escape from immune control and form clinically detectable tumors. Tetraploidy, which consists in the intrinsically unstable duplication of the genome, is considered as a (pre)-cancerous event that can result in aneuploidy and contribute to oncogenesis. We previously described the fact that tetraploid cells can be eliminated by the immune system. Here, we investigate the role of different innate and acquired immune effectors by inoculating hyperploid cancer cells into wild type or mice bearing different immunodeficient genotypes (Cd1d-/-, FcRn-/-, Flt3l-/-, Foxn1nu/nu, MyD88-/-, Nlrp3-/-, Ighmtm1Cgn, Rag2-/-), followed by the monitoring of tumor incidence, growth and final ploidy status. Our results suggest that multiple different immune effectors including B, NK, NKT and T cells, as well as innate immune responses involving the interleukine-1 receptor and the Toll-like receptor systems participate to the immunoselection against hyperploid cells. Hence, optimal anticancer immunosurveillance likely involves the contribution of multiple arms of the immune system.

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Citations

Mar 3, 2020·Frontiers in Immunology·Sara SaabHumam Kadara
Feb 23, 2021·Frontiers in Immunology·Ting-Yi LinChia-Yang Li
Aug 24, 2021·Frontiers in Cell and Developmental Biology·Eric HengKezhong Zhang
Nov 3, 2021·Cell Death & Disease·Jiayin DengLaura Senovilla

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