The Roles of Pyroptosis in Tumor Immune Microenvironment and Tumor Immunotherapy

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 30 June 2024 | Viewed by 1933

Special Issue Editors

Department of Biology, Chemistry, Pharmacy, Free University of Berlin, Berlin, Germany
Interests: experimental pharmacology and cancer immunotherapy

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Guest Editor
Department of Molecular Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, MA, USA
Interests: obesity; metabolic disorders; diabetes; immunogenic cell death; combination therapy

Special Issue Information

Dear Colleagues,

Pyroptosis was long regarded as caspase-1-mediated monocyte death in response to certain bacterial insults. Caspase-1 is activated upon various infectious and immunological challenges through different inflammasomes. The discovery of caspase-11/4/5 function in sensing intracellular lipopolysaccharide expands the spectrum of pyroptosis mediators and also reveals that pyroptosis is not cell-type specific. Recent studies have identified the pyroptosis executioner, gasdermin D (GSDMD), a substrate of both caspase-1 and caspase-11/4/5. GSDMD represents a large gasdermin family bearing a novel membrane pore-forming activity. Thus, pyroptosis has been redefined as gasdermin-mediated programmed necrosis. Tumor immune microenvironment (TIME) includes tumor cells, immune cells, cytokines, etc. The interactions between these components, which are divided into anti-tumor and pro-tumor, determine the trend of anti-tumor immunity. Although the immune system can eliminate tumors through the cancer-immune cycle, tumors appear to eventually evade immune surveillance by shaping an immunosuppressive microenvironment. Immunotherapy reshapes the TIME and restores the tumor-killing ability of anti-tumor immune cells. Pyroptosis represents the newly discovered immunogenic cell death (ICD) forms. Promoting ICD may alter the tumor microenvironment (TME) and the influx of tumor-infiltrating lymphocytes (TILs). Combining their inducers and immune checkpoint inhibitors (ICIs) is synergistic in enhancing antitumor effects.

The goal of this Special Issue is to provide a forum to advance research on the contribution of pyroptosis of tumor cells to the reconstruction of tumor immune microenvironment, which further influences the progression of various diseases. Additionally, these novel findings could be used to develop approaches for the diagnosis, treatment, and prognosis of cancer.

Original research articles, methods, reviews, and mini reviews are welcome. Specific areas of interest for thise Special Issue include, but are not limited to, the following:

  • Mechanisms of pyroptosis in cancer cells;
  • Association between pyroptosis of tumor cells and immune cell infiltration;
  • Combination therapy of tumor cells pyroptosis inducers and tumor immunity;
  • Pathways of pyroptosis and prognostic model of cancers;
  • Impact of pyroptosis of tumor cells on cancer immunotherapy;
  • Cancer biotherapy (gene therapy, cell therapy, mRNA, peptides, etc.) targeting pyroptosis pathway;
  • Nanomedicine for cancers based on pyroptosis pathways.

Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of the scope for this section and will not be accepted as part of this Special Issue.

Dr. Chen Li
Dr. Lei Huang
Guest Editors

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Keywords

  • pyroptosis
  • tumor immune microenvironment
  • tumor immunotherapy
  • inflammation
  • programmed cell death

Published Papers (1 paper)

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Review

34 pages, 1503 KiB  
Review
Cell Death in Liver Disease and Liver Surgery
by Christian Stoess, Yeon-Kyung Choi, Janset Onyuru, Helmut Friess, Hal M. Hoffman, Daniel Hartmann and Ariel E. Feldstein
Biomedicines 2024, 12(3), 559; https://doi.org/10.3390/biomedicines12030559 - 01 Mar 2024
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Abstract
Cell death is crucial for maintaining tissue balance and responding to diseases. However, under pathological conditions, the surge in dying cells results in an overwhelming presence of cell debris and the release of danger signals. In the liver, this gives rise to hepatic [...] Read more.
Cell death is crucial for maintaining tissue balance and responding to diseases. However, under pathological conditions, the surge in dying cells results in an overwhelming presence of cell debris and the release of danger signals. In the liver, this gives rise to hepatic inflammation and hepatocellular cell death, which are key factors in various liver diseases caused by viruses, toxins, metabolic issues, or autoimmune factors. Both clinical and in vivo studies strongly affirm that hepatocyte death serves as a catalyst in the progression of liver disease. This advancement is characterized by successive stages of inflammation, fibrosis, and cirrhosis, culminating in a higher risk of tumor development. In this review, we explore pivotal forms of cell death, including apoptosis, pyroptosis, and necroptosis, examining their roles in both acute and chronic liver conditions, including liver cancer. Furthermore, we discuss the significance of cell death in liver surgery and ischemia-reperfusion injury. Our objective is to illuminate the molecular mechanisms governing cell death in liver diseases, as this understanding is crucial for identifying therapeutic opportunities aimed at modulating cell death pathways. Full article
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