Abstract
Engagement of CD137 receptor by agonistic monoclonal antibodies (mAb) stimulates IFN-gamma production and eradicates established tumors in syngeneic mouse models. Using IFN-gamma-deficient mice or neutralizing mAb, we demonstrate that IFN-gamma is an absolute requirement for the antitumor effect of CD137 mAb. Despite progressive tumor growth in IFN-gamma-depleted mice, a fully competent CD8(+) cytolytic T cell (CTL) response developed in the lymph nodes. In addition, tumor cell sensitivity to IFN-gamma was not required because expression of a dominant-negative IFN-gamma receptor on the tumor did not affect the therapeutic effect of CD137 mAb. However, in the absence of IFN-gamma, the number of tumor-infiltrating CD8(+) CTLs was drastically decreased. Our results demonstrate that IFN-gamma is a critical factor regulating the infiltration of antigen-specific CTL into the tumor.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Antibodies, Monoclonal / immunology
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Antibodies, Monoclonal / pharmacology*
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Antigens, CD
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Cell Line, Transformed
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DNA-Binding Proteins*
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Epitopes, T-Lymphocyte / immunology
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Female
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Interferon-gamma / immunology*
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Lymph Nodes / immunology*
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Lymphocyte Activation / immunology
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Lymphocytes, Tumor-Infiltrating / immunology*
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Mice
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Mice, Inbred C57BL
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Neoplasms, Experimental / immunology
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Neoplasms, Experimental / therapy
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Oncogene Proteins, Viral / immunology
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Receptors, Nerve Growth Factor / immunology*
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Receptors, Tumor Necrosis Factor / immunology*
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T-Lymphocytes, Cytotoxic / immunology*
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Tumor Necrosis Factor Receptor Superfamily, Member 9
Substances
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Antibodies, Monoclonal
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Antigens, CD
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DNA-Binding Proteins
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E7 protein, Human papillomavirus type 18
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Epitopes, T-Lymphocyte
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Oncogene Proteins, Viral
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Receptors, Nerve Growth Factor
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Receptors, Tumor Necrosis Factor
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TNFRSF9 protein, human
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Tnfrsf9 protein, mouse
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Tumor Necrosis Factor Receptor Superfamily, Member 9
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Interferon-gamma