Abstract
Abstract Group 2 innate lymphoid cells (ILC2) are essential to maintain tissue homeostasis. In cancer, ILC2 can harbor both pro- and anti-tumorigenic functions but the mechanisms underpinning the execution of paradoxical outcomes is not known, nor how it affects clinical outcomes for tumors such as melanoma. We begin to unravel how ILC2 infiltrate human melanoma tumors and execute their anti-tumor potential through a variety of cytokines such granulocyte-macrophage colony-stimulating factor (GM-CSF) to coordinate the recruitment and activation of eosinophils to enhance the anti-tumor response. We identify cytokine-inhibitory receptor circuits that concurrently both promote and limit ILC2 function. Significantly, by understanding these hubs can break the negative impact of ILC2 through specific targetting to limit ILC2 promotion of tumor growth. Together, our results identified ILC2 as a critical immune cell type involved in melanoma immunity and revealed an as yet untapped synergistic approach to harness ILC2 function for anti-tumor immunotherapies.
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