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Editorial

NK cells beat T cells at early breast cancer control

, , , ORCID Icon & ORCID Icon
Article: 1806010 | Received 20 Jul 2020, Accepted 31 Jul 2020, Published online: 23 Aug 2020

Figures & data

Figure 1. Failing NK cell immunosurveillance may reveal novel immunotherapeutic approaches for luminal B breast cancer. Endogenous mammary carcinomas driven in immunocompetent C57BL/6 female mice by 7,12-dimethylbenz[a]anthracene (DMBA) and medroxyprogesterone acetate (MPA) – a model of luminal B breast cancer in women – are under early immunosurveillance by natural killer (NK) cells, not CD8+ cytotoxic T cells. This observation raises the interesting and hitherto untested possibility that agents targeting NK cells, including recombinant interleukin 15 (rIL-15) and antibodies blocking killer cell lectin like receptor C1 (KLRC1, best known as NKG2A), may mediate therapeutic activity not only against DMBA/MPA-driven tumors in mice, but also against luminal B breast cancers in women. That said, the adaptive immune system of mice bearing DMBA/MPA-driven tumors has not lost the ability to mount tumor-targeting responses upon administration of immunostimulatory chemotherapeutics or caloric restriction mimetics (CRMs). TREG, regulatory T.

Figure 1. Failing NK cell immunosurveillance may reveal novel immunotherapeutic approaches for luminal B breast cancer. Endogenous mammary carcinomas driven in immunocompetent C57BL/6 female mice by 7,12-dimethylbenz[a]anthracene (DMBA) and medroxyprogesterone acetate (MPA) – a model of luminal B breast cancer in women – are under early immunosurveillance by natural killer (NK) cells, not CD8+ cytotoxic T cells. This observation raises the interesting and hitherto untested possibility that agents targeting NK cells, including recombinant interleukin 15 (rIL-15) and antibodies blocking killer cell lectin like receptor C1 (KLRC1, best known as NKG2A), may mediate therapeutic activity not only against DMBA/MPA-driven tumors in mice, but also against luminal B breast cancers in women. That said, the adaptive immune system of mice bearing DMBA/MPA-driven tumors has not lost the ability to mount tumor-targeting responses upon administration of immunostimulatory chemotherapeutics or caloric restriction mimetics (CRMs). TREG, regulatory T.