Restoring the Immunity in the Tumor Microenvironment: Insights into Immunogenic Cell Death in Onco-Therapies

Hernández, Ángela-Patricia; Juanes-Velasco, Pablo; Landeira-Viñuela, Alicia; Bareke, Halin; Montalvillo, Enrique; Góngora, Rafael; Fuentes, Manuel

doi:10.3390/cancers13112821

Cited by 37 publications

(23 citation statements)

References 177 publications

(217 reference statements)

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“… 234 Other representative DAMPs released by ICD and molecular mechanisms for DAMP-mediated activation of the immune system in TME have been elaborated in detail by Hernández et al, etc. 236 …”

Section: Pyroptosis Synergizes Antitumor Immune Responsementioning

confidence: 99%

Autophagy, ferroptosis, pyroptosis, and necroptosis in tumor immunotherapy

Gao

Wang

Zhou

et al. 2022

Sig Transduct Target Ther

466

189

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In recent years, immunotherapy represented by immune checkpoint inhibitors (ICIs) has led to unprecedented breakthroughs in cancer treatment. However, the fact that many tumors respond poorly or even not to ICIs, partly caused by the absence of tumor-infiltrating lymphocytes (TILs), significantly limits the application of ICIs. Converting these immune “cold” tumors into “hot” tumors that may respond to ICIs is an unsolved question in cancer immunotherapy. Since it is a general characteristic of cancers to resist apoptosis, induction of non-apoptotic regulated cell death (RCD) is emerging as a new cancer treatment strategy. Recently, several studies have revealed the interaction between non-apoptotic RCD and antitumor immunity. Specifically, autophagy, ferroptosis, pyroptosis, and necroptosis exhibit synergistic antitumor immune responses while possibly exerting inhibitory effects on antitumor immune responses. Thus, targeted therapies (inducers or inhibitors) against autophagy, ferroptosis, pyroptosis, and necroptosis in combination with immunotherapy may exert potent antitumor activity, even in tumors resistant to ICIs. This review summarizes the multilevel relationship between antitumor immunity and non-apoptotic RCD, including autophagy, ferroptosis, pyroptosis, and necroptosis, and the potential targeting application of non-apoptotic RCD to improve the efficacy of immunotherapy in malignancy.

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Section: Pyroptosis Synergizes Antitumor Immune Responsementioning

confidence: 99%

Autophagy, ferroptosis, pyroptosis, and necroptosis in tumor immunotherapy

Gao

Wang

Zhou

et al. 2022

Sig Transduct Target Ther

466

189

View full text Add to dashboard Cite

show abstract

“…At late time point of cell death, tumor cells can transfer “eat me signals” to facilitate immune cells phagocytosis and tumor antigen presentation, resulting in the conversion of dying tumor cells to adjuvanted-endogenous tumor vaccines ( 49 ). The nature of DAMPs is the fundamentally dynamic responding to chemotherapy-elicited cell stress that involve in multifaceted influences on extra- and intracellular microenvironments ( 50 ).…”

Section: Enhancing the Antigenicity Or Adjuvanticity Of Bc Cellsmentioning

confidence: 99%

Immunostimulatory Properties of Chemotherapy in Breast Cancer: From Immunogenic Modulation Mechanisms to Clinical Practice

et al. 2022

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Breast cancer (BC) is the most common malignancy among females. Chemotherapy drugs remain the cornerstone of treatment of BC and undergo significant shifts over the past 100 years. The advent of immunotherapy presents promising opportunities and constitutes a significant complementary to existing therapeutic strategies for BC. Chemotherapy as a cytotoxic treatment that targets proliferation malignant cells has recently been shown as an effective immune-stimulus in multiple ways. Chemotherapeutic drugs can cause the release of damage-associated molecular patterns (DAMPs) from dying tumor cells, which result in long-lasting antitumor immunity by the key process of immunogenic cell death (ICD). Furthermore, Off-target effects of chemotherapy on immune cell subsets mainly involve activation of immune effector cells including natural killer (NK) cells, dendritic cells (DCs), and cytotoxic T cells, and depletion of immunosuppressive cells including Treg cells, M2 macrophages and myeloid-derived suppressor cells (MDSCs). Current mini-review summarized recent large clinical trials regarding the combination of chemotherapy and immunotherapy in BC and addressed the molecular mechanisms of immunostimulatory properties of chemotherapy in BC. The purpose of our work was to explore the immune-stimulating effects of chemotherapy at the molecular level based on the evidence from clinical trials, which might be a rationale for combinations of chemotherapy and immunotherapy in BC.

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“…Tumors maintain the microenvironment of immune suppression by displaying low immunogenicity and secreting immunosuppressive cytokines, including IL-10, TGF-β, and VEGF ( 168 ). ICD can be triggered by various treatments, such as chemotherapy, RT and photodynamic therapy ( 169 ). Various cell death-related molecules, such as damage-associated molecular patterns, are released to enhance the immunogenicity of tumor cells and the initial immune response, which is an innovative measure in immunotherapy ( 169 ).…”

Section: Ros and Tmementioning

confidence: 99%

“…ICD can be triggered by various treatments, such as chemotherapy, RT and photodynamic therapy ( 169 ). Various cell death-related molecules, such as damage-associated molecular patterns, are released to enhance the immunogenicity of tumor cells and the initial immune response, which is an innovative measure in immunotherapy ( 169 ). At present, the prevailing notion is that there is a positive association between ROS production and ICD induction in anti-tumor therapy ( 170 ).…”

Section: Ros and Tmementioning

confidence: 99%

Role of reactive oxygen species in tumors based on the ‘seed and soil’ theory: A complex interaction (Review)

Liang

et al. 2021

Oncol Rep

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Tumor microenvironment (TME) can serve as the 'soil' for the growth and survival of tumor cells and function synergically with tumor cells to mediate tumor progression and therapeutic resistance. Reactive oxygen species (ROS) is somewhat of a double-edged sword for tumors. Accumulating evidence has reported that regulating ROS levels can serve an anti-tumor role in the TME, including the promotion of cancer cell apoptosis, inhibition of angiogenesis, preventing immune escape, manipulating tumor metabolic reorganization and improving drug resistance. In the present review, the potential role of ROS in anti-tumor therapy was summarized, including the possibility of directly or indirectly targeting the TME. Contents 1. Introduction 2. ROS and TME 3. ROS and tumor drug resistance 4. Conclusions

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Restoring the Immunity in the Tumor Microenvironment: Insights into Immunogenic Cell Death in Onco-Therapies

Cited by 37 publications

References 177 publications

Autophagy, ferroptosis, pyroptosis, and necroptosis in tumor immunotherapy

Autophagy, ferroptosis, pyroptosis, and necroptosis in tumor immunotherapy

Immunostimulatory Properties of Chemotherapy in Breast Cancer: From Immunogenic Modulation Mechanisms to Clinical Practice

Role of reactive oxygen species in tumors based on the ‘seed and soil’ theory: A complex interaction (Review)

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