PuSH - Publication Server of Helmholtz Zentrum München: TNFR1 signaling and IFN-gamma signaling determine whether T cells induce tumor dormancy or promote multistage carcinogenesis.

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Müller-Hermelink, N.* ; Braumüller, H.* ; Pichler, B.* ; Wieder, T.* ; Mailhammer, R. ; Schaak, K.* ; Ghoreschi, K.* ; Yazdi, A.* ; Haubner, R.* ; Sander, CA.* ; Mocikat, R. ; Schwaiger, M.* ; Förster, I.* ; Huss, R.* ; Weber, WA.* ; Kneilling, M.* ; Röcken, M.*

TNFR1 signaling and IFN-gamma signaling determine whether T cells induce tumor dormancy or promote multistage carcinogenesis.

Cancer Cell 13, 507-518 (2008)

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Open Access Green as soon as Postprint is submitted to ZB.

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Immune responses may arrest tumor growth by inducing tumor dormancy. The mechanisms leading to either tumor dormancy or promotion of multistage carcinogenesis by adaptive immunity are poorly characterized. Analyzing T antigen (Tag)-induced multistage carcinogenesis in pancreatic islets, we show that Tag-specific CD4+ T cells home selectively into the tumor microenvironment around the islets, where they either arrest or promote transition of dysplastic islets into islet carcinomas. Through combined TNFR1 signaling and IFN-gamma signaling, Tag-specific CD4+ T cells induce antiangiogenic chemokines and prevent alpha(v)beta(3) integrin expression, tumor angiogenesis, tumor cell proliferation, and multistage carcinogenesis, without destroying Tag-expressing islet cells. In the absence of either TNFR1 signaling or IFN-gamma signaling, the same T cells paradoxically promote angiogenesis and multistage carcinogenesis. Thus, tumor-specific T cells can directly survey multistage carcinogenesis through cytokine signaling.

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