Growth by Inducing Angiogenesis Receptor Immune Interaction Promotes Tumor
نویسندگان
چکیده
Growth of solid fibrosarcoma tumors in mice was inhibited by the release of a soluble lymphotoxinreceptor inhibitor (LT R-immunoglobulin fusion protein) from the tumor cells. Tumor growth arrest in mice deficient in the ligand LT 1 2 demonstrated the requirement for activation of the LT R on the tumor cells by host cell-derived LT 1 2. Activation of the LT R resulted in enhanced release of macrophage inflammatory protein-2. Blocked angiogenesis was revealed in LT R inhibitor-producing tumor nodules by immunohistochemistry and in vivo microscopy. The growth arrest of LT R inhibitor-producing fibrosarcomas was overcome by forced MIP-2 expression in the tumor cells. Thus, LT R activation on tumor cells by activated host lymphocytes can initiate a novel proangiogenic pathway leading to organized tumor tissue development.
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