Abstract：
: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 antigen-presenting 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.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Ma Y,Mattarollo SR,Adjemian S,Yang H,Aymeric L,Hannani D,Portela Catani JP,Duret H,Teng MW,Kepp O,Wang Y,Sistigu A,Schultze JL,Stoll G,Galluzzi L,Zitvogel L,Smyth MJ,Kroemer Gdoi
10.1158/0008-5472.CAN-13-1265subject
Has Abstractpub_date
2014-01-15 00:00:00pages
436-45issue
2eissn
0008-5472issn
1538-7445pii
0008-5472.CAN-13-1265journal_volume
74pub_type
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