A critical requirement of interferon γ-mediated angiostasis for tumor rejection by CD8+ T cells

• Published in: Cancer research (Chicago, Ill.) Ill.), 2003-07, Vol.63 (14), p.4095-4100
• Main Authors: ZHIHAI QIN, SCHWARTZKOPFF, Johannes, PRADERA, Felicia, KAMMERTOENS, Thomas, SELIGER, Barbara, PIRCHER, Hanspeter, BLANKENSTEIN, Thomas
• Format: Article
• Language: English
• Subjects: 3T3 Cells; Animals; Biological and medical sciences; CD8-Positive T-Lymphocytes - immunology; CD8-Positive T-Lymphocytes - metabolism; Fibrosarcoma - blood supply; Fibrosarcoma - immunology; Fibrosarcoma - therapy; Host-tumor relations. Immunology. Biological markers; Immunization; Immunotherapy, Adoptive - methods; Interferon-gamma - biosynthesis; Interferon-gamma - immunology; Medical sciences; Melanoma, Experimental - blood supply; Melanoma, Experimental - immunology; Melanoma, Experimental - therapy; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Mice, Inbred DBA; Neoplasms, Experimental - blood supply; Neoplasms, Experimental - immunology; Neoplasms, Experimental - therapy; Neovascularization, Pathologic - immunology; Neovascularization, Pathologic - prevention & control; Tumors
• ISSN: 0008-5472; 1538-7445

It is thought that tumor rejection by CD8(+) T-cell effectors is primarily mediated by direct killing. We show that rejection of different tumors (fibrosarcoma, ras-transformed fibroblasts, colon carcinoma, and plasmacytoma) by CD8(+) T cells is always preceded by inhibition of tumor-induced angiogenesis. Angiostasis and tumor rejection were observed in perforin but not in IFN-gamma-deficient mice. Furthermore, adoptive transfer of tumor-specific CD8(+) T cells from IFN-gamma-competent mice inhibited angiogenesis of lung metastases in comparison to those from IFN-gamma gene-deficient mice. Taken together with our previous findings, we conclude that IFN-gamma-dependent antiangiogenesis is a general mechanism involved in tumor rejection by CD4(+) and CD8(+) T-cell effectors.