Chemotherapy-triggered cathepsin B release in myeloid-derived suppressor cells activates the Nlrp3 inflammasome and promotes tumor growth

By M. Bruchard, G. Mignot, V. Derangère, Fanny Chalmin, Angélique Chevriaux, F. Végran, W. Boireau, B. Simon, B. Ryffel, J. Connat and 5 more. Nature Medicine, 2012

726 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/38cd2a7648b1464086066549ff7f86b54389be2f

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Citations in the corpus

Macrophage regulation of tumor responses to anticancer therapies. (2013, background): “In this regard, a recent study showed that two broadly used chemotherapeutics, gemcitabine and 5-fluorouracil, induce monocytes/MDSCs to release cathepsin B from lysosomes (Bruchard et al., 2013).”
Mechanism of action of conventional and targeted anticancer therapies: reinstating immunosurveillance. (2013, background): “…by DCs is required for anticancer immune responses (Ghiringhelli et al., 2009; Mattarollo et al., 2011), yet can improve the therapeutic potential of 5-fluorouracil and gemcitabine, because IL-1b produced by MDSCs can participate in tumor-promoting inflammatory reactions (Bruchard et al., 2013).”
Immune-based mechanisms of cytotoxic chemotherapy: implications for the design of novel and rationale-based combined treatments against cancer (2013, background): “pro-tumorigenic cytokines via inflammasome pathways, thus limiting the therapeutic efficacy of the drugs.(66)”
The interaction of anticancer therapies with tumor-associated macrophages (2015, background): “…TAMs by CSF-1 (DeNardo et al., 2011), protumor polarization (Dijkgraaf et al., 2013; Pyonteck et al., 2013), activation via IL-1 of a tumor-promoting Th17 response (Bruchard et al., 2013), and protection against chemotherapy toxicity of CSCs (Jinushi et al., 2011; Mitchem et al., 2013).”
Immunological Effects of Conventional Chemotherapy and Targeted Anticancer Agents. (2015, background): “Immunological Effects of Targeted Anticancer Agents Agent Setting Effect Notes Reference Bevacizumab transplantable murine CRC depletes TREG cells mechanism involving KDR Terme et al., 2013 Dasatinib CML favors the expansion of circulating CTLs and NK cells correlates with molecular response to chem”
Macrophages and therapeutic resistance in cancer (2015, positive): “A possible underlying mechanism may derive from the cathepsin B-dependent activation of inflammasomes in myeloid cells following treatment with gemcitabine or fluorouracil, leading to IL-1b release and enhancement of a TH17 immune response (Bruchard et al., 2013).”
Myeloid derived suppressor cells (2013, background): “It was recently discovered that the efficacy of 5-FU therapy is limited by induction of Nlrp3 inflammasome, leading to MDSC-derived IL-1beta secretion and induction of angiogenesis, suggesting that combination of 5-FU with anti-IL1beta or Nlrp3 inflammasome inhibitors to increase therapeutic potenti”