CD4+ T cell-mediated tumor rejection involves inhibition of angiogenesis that is dependent on IFNgamma receptor expression by nonhematopoietic cells

Immunity against MHC class II- tumors can be mediated by CD4+ T cells in the effector phase through an unknown mechanism. We show that this is IFNγ dependent but does not require IFN{gamma} receptor (IFNγR) expression on tumor cells, T cells, or other hematopoietic cells and that IFN{gamma}R expression is not necessary in the priming phase. However, tumor immunity requires IFN{gamma}R expression on nonhematopoietic cells in the effector phase and involves inhibition of tumor-induced angiogenesis. This shows that an effective anti-tumor response involves communication between CD4+ T cells and nonhematopoietic cells, most likely within the tumor stroma, and that tumor immunity must not entirely rely on direct tumor cell killing.