Journal ArticleDOI
Autophagy-dependent anticancer immune responses induced by chemotherapeutic agents in mice.
Mickaël Michaud,Mickaël Michaud,Mickaël Michaud,Isabelle Martins,Isabelle Martins,Isabelle Martins,Abdul Qader Sukkurwala,Abdul Qader Sukkurwala,Abdul Qader Sukkurwala,Sandy Adjemian,Sandy Adjemian,Sandy Adjemian,Yuting Ma,Patrizia Pellegatti,Shensi Shen,Shensi Shen,Shensi Shen,Oliver Kepp,Oliver Kepp,Oliver Kepp,Marie Scoazec,Grégoire Mignot,Santiago Rello-Varona,Santiago Rello-Varona,Santiago Rello-Varona,Maximilien Tailler,Maximilien Tailler,Maximilien Tailler,Laurie Menger,Laurie Menger,Laurie Menger,Erika Vacchelli,Erika Vacchelli,Erika Vacchelli,Lorenzo Galluzzi,Lorenzo Galluzzi,Lorenzo Galluzzi,François Ghiringhelli,Francesco Di Virgilio,Laurence Zitvogel,Guido Kroemer +40 more
TLDR
It is demonstrated that autophagy, which is often disabled in cancer, is dispensable for chemotherapy-induced cell death but required for its immunogenicity, and increased extracellular ATP concentrations improve the efficacy of antineoplastic chemotherapies when Autophagy is disabled.Abstract:
Antineoplastic chemotherapies are particularly efficient when they elicit immunogenic cell death, thus provoking an anticancer immune response. Here we demonstrate that autophagy, which is often disabled in cancer, is dispensable for chemotherapy-induced cell death but required for its immunogenicity. In response to chemotherapy, autophagy-competent, but not autophagy-deficient, cancers attracted dendritic cells and T lymphocytes into the tumor bed. Suppression of autophagy inhibited the release of adenosine triphosphate (ATP) from dying tumor cells. Conversely, inhibition of extracellular ATP-degrading enzymes increased pericellular ATP in autophagy-deficient tumors, reestablished the recruitment of immune cells, and restored chemotherapeutic responses but only in immunocompetent hosts. Thus, autophagy is essential for the immunogenic release of ATP from dying cells, and increased extracellular ATP concentrations improve the efficacy of antineoplastic chemotherapies when autophagy is disabled.read more
Citations
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Journal ArticleDOI
Autophagy, autophagy-associated adaptive immune responses and its role in hematologic malignancies
TL;DR: Based on the successful experimental findings in vitro and in vivo, clinical trials of autophagy inhibitor such as hydroxychloroquine in combination with chemotherapy in patients with blood cancers are currently underway, however, Autophagy inactivation might impair autophagic-triggered anticancer immunity, whereas induction of autphagy might become an effective immunotherapy.
Journal ArticleDOI
An Injectable Hydrogel Reshaping Adenosinergic Axis for Cancer Therapy
TL;DR: Different from the A2A adenosine receptor blockade, this strategy achieves a cascade amplification of ATP‐based anti‐tumor immune response, enabling strong immunogenicity along with reversing the negative feedback of adenosinergic axis for powerfully suppressing tumor progression.
Journal ArticleDOI
The protease activity of human ATG4B is regulated by reversible oxidative modification.
TL;DR: A novel molecular mechanism that oxidative modification at Cys292 and Cys361 sites regulates ATG4B function, which modulates autophagy, which reveals increased autophagic flux and decreased oxidation sensitivity.
Patent
Treatment of autophagy-based disorders and related pharmaceutical compositions, diagnostic and screening assays and kits
Vojo Deretic,Eliseo F. Castillo +1 more
TL;DR: In this paper, a method for treating a subject suffering from a Mycobacterium infection by administering to the subject a therapeutically-effective amount of a degradative autophagy agonist or a secretory autoophagy antagonist was described.
Journal ArticleDOI
Ligustilide inhibits the activation of cancer-associated fibroblasts.
Jing Ma,Yuwei Xu,Qilin Zheng,Yuanyuan Wang,Minghua Hu,Fangli Ma,Hanan Long,Zhihai Qin,Ning Tao +8 more
TL;DR: It is found that ligustilide had no effect on the growth of splenocytes but that it could change the immunosuppressive function of CAFs through the TLR4‐NF‐&kgr;B pathway and restore T‐cell proliferation previously inhibited by the CAF supernatant.
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Calreticulin exposure dictates the immunogenicity of cancer cell death
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TL;DR: A functional classification of cell death subroutines is proposed that applies to both in vitro and in vivo settings and includes extrinsic apoptosis, caspase-dependent or -independent intrinsic programmed cell death, regulated necrosis, autophagic cell death and mitotic catastrophe.
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