Lymphotoxin-beta receptor immune interaction promotes tumor growth by inducing angiogenesisстатья
Статья опубликована в высокорейтинговом журнале
Информация о цитировании статьи получена из
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Статья опубликована в журнале из списка Web of Science и/или Scopus
Дата последнего поиска статьи во внешних источниках: 16 декабря 2014 г.
Аннотация:Growth of solid fibrosarcoma tumors in mice was inhibited by the release of a solublelymphotoxin-β receptor inhibitor (LTβR-immunoglobulin fusion protein) from the tumor cells. Tumor growth arrest in mice deficient in the ligand LTα1β2 demonstrated the requirement for activation of the LTβR on the tumor cells by host cell-derived LTα1β2. Activation of the LTβR resulted in enhanced release of macrophage inflammatory protein-2. Blocked angiogenesis was revealed in LTβR inhibitor-producing tumor nodules by immunohistochemistry and in vivo microscopy. The growth arrest of LTβR inhibitor-producing fibrosarcomas was overcome by forced MIP-2 expression in the tumor cells. Thus, LTβR activation on tumor cells by activated host lymphocytes can initiate a novel proangiogenic pathway leading to organized tumor tissue development.