Abstract
Abstract Cancer immunoediting is the process whereby immune cells protect against cancer formation and sculpt the immunogenicity of developing tumors. The complete process of immunoediting requires both innate and adaptive immunity, but it remains unclear to what extent innate immunity alone is capable of immunoediting. To determine whether the innate immune system can edit tumor cells in the absence of adaptive immunity, we compared the incidence and immunogenicity of 3’methylcholanthrene-induced sarcomas in syngeneic wild-type, RAG2-/-, and RAG2-/-x γc-/- mice. We found that innate immune cells could indeed manifest cancer immunoediting activity in the absence of adaptive immunity. This activity required γc and IFNγ, which mediated the induction of M1 macrophages. M1 macrophages could be elicited by administration of CD40 agonists, thereby restoring editing activity in RAG2-/-x γc-/- mice. Our results suggest that in the absence of adaptive immunity, natural killer cell production of IFNγ induces M1 macrophages, which act as important effectors during cancer immunoediting.
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