CCL2/CCR2-Dependent Recruitment of Functional AntigenPresenting Cells into Tumors upon Chemotherapy
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109
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article
Data de publicação
2014
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AMER ASSOC CANCER RESEARCH
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MA, Yuting
MATTAROLLO, Stephen R.
ADJEMIAN, Sandy
YANG, Heng
AYMERIC, Laetitia
HANNANI, Dalil
DURET, Helene
TENG, Michele W. L.
KEPP, Oliver
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Citação
CANCER RESEARCH, v.74, n.2, p.436-445, 2014
Resumo
The therapeutic efficacy of anthracyclines relies, at least partially, on the induction of a dendritic cell-and T-lymphocyte-dependent anticancer immune response. Here, we show that anthracycline-based chemotherapy promotes the recruitment of functional CD11b(+)CD11c(+)Ly6C(high)Ly6G(-)MHCII(+) dendritic cell-like antigenpresenting cells (APC) into the tumor bed, but not into lymphoid organs. Accordingly, draining lymph nodes turned out to be dispensable for the proliferation of tumor antigen-specific T cells within neoplastic lesions as induced by anthracyclines. In addition, we found that tumors treated with anthracyclines manifest increased expression levels of the chemokine Ccl2. Such a response is important as neoplasms growing in Ccl2(-/-) mice failed to accumulate dendritic cell-like APCs in response to chemotherapy. Moreover, cancers developing in mice lacking Ccl2 or its receptor (Ccr2) exhibited suboptimal therapeutic responses to anthracycline-based chemotherapy. Altogether, our results underscore the importance of the CCL2/CCR2 signaling axis for therapeutic anticancer immune responses as elicited by immunogenic chemotherapy. (C) 2013 AACR.
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Referências
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