Contribution of humoral immune responses to the antitumor effects mediated by anthracyclines

Hannani, D., Locher, C., Yamazaki, T., Colin-Minard, V., Vetizou, M., Aymeric, L., Viaud, S., Sanchez, D., Smyth, M. J., Bruhns, P., Kroemer, G. and Zitvogel, L. (2014) Contribution of humoral immune responses to the antitumor effects mediated by anthracyclines. Cell Death and Differentiation, 21 1: 50-58. doi:10.1038/cdd.2013.60


Author Hannani, D.
Locher, C.
Yamazaki, T.
Colin-Minard, V.
Vetizou, M.
Aymeric, L.
Viaud, S.
Sanchez, D.
Smyth, M. J.
Bruhns, P.
Kroemer, G.
Zitvogel, L.
Title Contribution of humoral immune responses to the antitumor effects mediated by anthracyclines
Journal name Cell Death and Differentiation   Check publisher's open access policy
ISSN 1350-9047
1476-5403
Publication date 2014-01
Year available 2013
Sub-type Article (original research)
DOI 10.1038/cdd.2013.60
Open Access Status
Volume 21
Issue 1
Start page 50
End page 58
Total pages 9
Place of publication London, United Kingdom
Publisher Nature
Collection year 2014
Language eng
Formatted abstract
Immunogenic cell death induced by cytotoxic compounds contributes to the success of selected chemotherapies by eliciting a protective anticancer immune response, which is mediated by CD4+ and CD8+ T cells producing interferon-γ. In many instances, cancer progression is associated with high titers of tumor-specific antibodies, which become detectable in the serum, but whose functional relevance is elusive. Here, we explored the role of humoral immune responses in the anticancer efficacy of anthracyclines. Chemotherapy reduced the number of tumor-infiltrating B cells, and failed to promote humoral responses against immunodominant tumor antigens. Although anthracycline-based anticancer chemotherapies failed in T cell-deficient mice, they successfully reduced the growth of cancers developing in mice lacking B lymphocytes (due to the injection of a B-cell-depleting anti-CD20 antibody), immunoglobulins (Igs) or Ig receptors (Fc receptor) due to genetic manipulations. These results suggest that the humoral arm of antitumor immunity is dispensable for the immune-dependent therapeutic effect of anthracyclines against mouse sarcoma. In addition, we show here that the titers of IgA and IgG antibodies directed against an autoantigen appearing at the cell surface of tumor cells post chemotherapy (calreticulin, CRT) did not significantly increase in patients treated with anthracyclines, and that anti-CRT antibodies had no prognostic or predictive significance. Collectively, our data indicate that humoral anticancer immune responses differ from cellular responses in, thus far, that they do not contribute to the success of anthracycline-mediated anticancer therapies in human breast cancers and mouse sarcomas.
Keyword Antibodies
Cancer
Chemotherapy
FcyR
Humoral immunity
Immunogenic cell death
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

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