To quickly adapt to changes in their environment, immune cells are highly plastic. However, the underlying mechanisms and the importance of NK cell plasticity for the development, progression and efficacy of immunotherapies in cancer remains elusive.

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We have recently shown that TGFβ-signaling drives phenotypic plasticity of NK cells in the TME (Gao et al. 2017). We observed that NK cells acquired an ILC1-like phenotype, which led to the immune escape of mouse tumors. Based on these findings, we seek to  (A) further  understand the cellular and molecular mechanisms contributing to NK cell plasticity and (B) advance our knowledge on the importance of ILC1-like cells for angiogenesis and myeloid cell recruitment in cancer.