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[Cancer Research 63, 4095-4100, July 15, 2003]
© 2003 American Association for Cancer Research

Immunology

A Critical Requirement of Interferon {gamma}-mediated Angiostasis for Tumor Rejection by CD8+ T Cells1

Zhihai Qin2, Johannes Schwartzkopff, Felicia Pradera, Thomas Kammertoens, Barbara Seliger, Hanspeter Pircher and Thomas Blankenstein

Institute of Immunology, University Clinic Benjamin-Franklin, Free University of Berlin, 12200 Berlin [Z. Q., T. B.]; Institute of Medical Microbiology and Hygiene, Department of Immunology, University of Freiburg, 79104 Freiburg [J. S., H. P.]; Max-Delbrück-Center for Molecular Medicine, 13092 Berlin [F. P., T. K., T. B.]; and Third Department of Internal Medicine, Johannes Gutenberg-University, 55131 Mainz [B. S.], Germany

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.




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