Cross-Talk between T Cells and Innate Immune Cells Is Crucial for IFN-γ-Dependent Tumor Rejection

Abstract

Though the importance of IFN-γ in tumor immunity has been well-demonstrated, little is known about its source and how it is induced. By using various bone marrow chimeric mice, we show here that IFN-γ essential for tumor immunity is solely produced by hemopoietic cells. Surprisingly, IFN-γ derived from T cells was not necessary for tumor immunity in this model. In the immunized mice, in which only innate immune cells have the IFN-γ-producing potential, tumors were efficiently rejected. The innate immune cells, such as NK1.1+ cells and CD11b+ cells, can provide sufficient amounts of IFN-γ which requires, however, the help of T cells. The close cooperation between T cells and innate immune cells during tumor regression is likely mediated by IL-2. Together, our results clearly illustrate how T cells cooperate with innate immune cells for IFN-γ-mediated tumor rejection and this may have important indications for clinical trials of tumor immunotherapy.