Natural killer cells contribute to 'hot' tumor regression in the allergic inflammatory environment.

Systemic immune status influences the elimination of tumor cells. However, it remains unclear how chronic inflammation in allergic diseases affects the tumor microenvironment and tumorigenesis. To investigate tumor progression in a state of heightened allergic inflammation, we established a mouse model of allergic inflammation. We used house dust mite extract to induce a hyper-reactive systemic immune response. Additionally, we subcutaneously inoculated two types of cancer cells (CT26 and 4T1 tumors). We conducted immune profiling of the ex-vivo tumor mass using multicolor flow cytometry staining and performed dynamic analysis of peripheral cytokines to explore the significant relationship between the development of allergic inflammation and tumorigenesis. We found that mice in a state of allergic inflammation were more susceptible to developing tumors. Interestingly, the growth of T cell-inflamed was inhibited in the allergic state, while growth of non-T cell-inflamed was promoted. Further research revealed that natural killer (NK) cells with enhanced tumor-killing or immune-regulating abilities were more active in " hot " tumors. Inhibiting NK cell activity can partially alleviate the impact of allergic inflammation on tumor growth. In summary, our results suggest that NK cells play significant role in suppressing tumor growth in an allergic inflammation mouse model. This phenomenon seems to be closely linked to both the inherent characteristics of the tumor and its interaction with the immune system. The innate immune system can be mobilized to synergize with the adaptive immune system to inhibit tumor growth, which opens a new way for a tumor immunotherapy.