Tumor necrosis factor is dispensable for the success of immunogenic anticancer chemotherapy
AuthorMa, Y; Yamazaki, T; Yang, H; Kepp, O; Galluzzi, L; Zitvogel, L; Smyth, MJ; Kroemer, G
PublisherTAYLOR & FRANCIS INC
University of Melbourne Author/sSMYTH, MARK
Document TypeJournal Article
CitationsMa, Y., Yamazaki, T., Yang, H., Kepp, O., Galluzzi, L., Zitvogel, L., Smyth, M. J. & Kroemer, G. (2013). Tumor necrosis factor is dispensable for the success of immunogenic anticancer chemotherapy. ONCOIMMUNOLOGY, 2 (6), https://doi.org/10.4161/onci.24786.
Access StatusOpen Access
The antineoplastic effects of anthracyclines have been shown to rely, at least in part, on a local immune response that involves dendritic cells (DCs) and several distinct subsets of T lymphocytes. Here, we show that the administration of anthracyclines to mice bearing established neoplasms stimulates the intratumoral secretion of tumor necrosis factor α (TNFα). However, blocking the TNFα/TNF receptor (TNFR) system by three different strategies-namely, (1) neutralizing antibodies, (2) etanercept, a recombinant protein in which TNFR is fused to the constant domain of an IgG1 molecule, and (3) gene knockout-failed to negatively affect the therapeutic efficacy of anthracyclines in three distinct tumor models. In particular, TNFα-blocking strategies did not influence the antineoplastic effects of doxorubicin (a prototypic anthracycline) against MCA205 fibrosarcomas growing in C57BL/6 mice, F244 sarcomas developing in 129/Sv hosts and H2N100 mammary carcinomas arising in BALB/c mice. These findings imply that, in contrast to other cytokines (such as interleukin-1β, interleukin-17 and interferon γ), TNFα is not required for anthracyclines to elicit therapeutic anticancer immune responses.
- Click on "Export Reference in RIS Format" and choose "open with... Endnote".
- Click on "Export Reference in RIS Format". Login to Refworks, go to References => Import References