CCL2/CCR2-dependent recruitment of functional antigen-presenting cells into tumors upon chemotherapy

Ma, Yuting, Mattarollo, Stephen R., Adjemian, Sandy, Yang, Heng, Aymeric, Laetitia, Hannani, Dalil, Portela Catani, Joao Paulo, Duret, Helene, Teng, Michele W. L., Kepp, Oliver, Wang, Yidan, Sistigu, Antonella, Schultze, Joachim L., Stoll, Gautier, Galluzzi, Lorenzo, Zitvogel, Laurence, Smyth, Mark J. and Kroemer, Guido (2014) CCL2/CCR2-dependent recruitment of functional antigen-presenting cells into tumors upon chemotherapy. Cancer Research, 74 2: 436-445. doi:10.1158/0008-5472.CAN-13-1265

Author Ma, Yuting
Mattarollo, Stephen R.
Adjemian, Sandy
Yang, Heng
Aymeric, Laetitia
Hannani, Dalil
Portela Catani, Joao Paulo
Duret, Helene
Teng, Michele W. L.
Kepp, Oliver
Wang, Yidan
Sistigu, Antonella
Schultze, Joachim L.
Stoll, Gautier
Galluzzi, Lorenzo
Zitvogel, Laurence
Smyth, Mark J.
Kroemer, Guido
Title CCL2/CCR2-dependent recruitment of functional antigen-presenting cells into tumors upon chemotherapy
Journal name Cancer Research   Check publisher's open access policy
ISSN 0008-5472
Publication date 2014-01-15
Year available 2013
Sub-type Article (original research)
DOI 10.1158/0008-5472.CAN-13-1265
Open Access Status Not yet assessed
Volume 74
Issue 2
Start page 436
End page 445
Total pages 10
Place of publication Philadelphia, PA, United States
Publisher American Association for Cancer Research
Language eng
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+ Ly6Chigh 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.
Keyword Oncology
Q-Index Code C1
Q-Index Status Confirmed Code
Grant ID Sonderforschungsbereich 704
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2014 Collection
School of Medicine Publications
UQ Diamantina Institute Publications
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