Ferroptosis, necroptosis, and pyroptosis in anticancer immunity DOI Creative Commons
Rong Tang, Jin Xu, Bo Zhang

et al.

Journal of Hematology & Oncology, Journal Year: 2020, Volume and Issue: 13(1)

Published: Aug. 10, 2020

Abstract In recent years, cancer immunotherapy based on immune checkpoint inhibitors (ICIs) has achieved considerable success in the clinic. However, ICIs are significantly limited by fact that only one third of patients with most types respond to these agents. The induction cell death mechanisms other than apoptosis gradually emerged as a new treatment strategy because tumors harbor innate resistance apoptosis. date, possibility combining two modalities not been discussed systematically. Recently, few studies revealed crosstalk between distinct and antitumor immunity. pyroptosis, ferroptosis, necroptosis combined showed synergistically enhanced activity, even ICI-resistant tumors. Immunotherapy-activated CD8+ T cells traditionally believed induce tumor via following main pathways: (i) perforin-granzyme (ii) Fas-FasL. identified mechanism which suppress growth inducing ferroptosis provoked review relationship system activation. Hence, this review, we summarize knowledge reciprocal interaction immunity mechanisms, particularly necroptosis, three potentially novel immunogenic death. Because evidence is derived from using animal models, also reviewed related bioinformatics data available for human tissues public databases, partially confirmed presence interactions activation

Language: Английский

The molecular machinery of regulated cell death DOI Creative Commons
Daolin Tang, Rui Kang, Tom Vanden Berghe

et al.

Cell Research, Journal Year: 2019, Volume and Issue: 29(5), P. 347 - 364

Published: April 4, 2019

Cells may die from accidental cell death (ACD) or regulated (RCD). ACD is a biologically uncontrolled process, whereas RCD involves tightly structured signaling cascades and molecularly defined effector mechanisms. A growing number of novel non-apoptotic forms have been identified are increasingly being implicated in various human pathologies. Here, we critically review the current state art regarding types RCD, including necroptosis, pyroptosis, ferroptosis, entotic death, netotic parthanatos, lysosome-dependent autophagy-dependent alkaliptosis oxeiptosis. The in-depth comprehension each these lethal subroutines their intercellular consequences uncover therapeutic targets for avoidance pathogenic loss.

Language: Английский

Citations

1992

Mitochondria as multifaceted regulators of cell death DOI
Florian J. Bock, Stephen W. G. Tait

Nature Reviews Molecular Cell Biology, Journal Year: 2019, Volume and Issue: 21(2), P. 85 - 100

Published: Oct. 21, 2019

Language: Английский

Citations

1894

Toll-like Receptors and the Control of Immunity DOI Creative Commons
Katherine A. Fitzgerald, Jonathan C. Kagan

Cell, Journal Year: 2020, Volume and Issue: 180(6), P. 1044 - 1066

Published: March 1, 2020

Language: Английский

Citations

1600

Pyroptosis: mechanisms and diseases DOI Creative Commons

Pian Yu,

Xu Zhang, Nian Liu

et al.

Signal Transduction and Targeted Therapy, Journal Year: 2021, Volume and Issue: 6(1)

Published: March 29, 2021

Abstract Currently, pyroptosis has received more and attention because of its association with innate immunity disease. The research scope expanded the discovery gasdermin family. A great deal evidence shows that can affect development tumors. relationship between tumors is diverse in different tissues genetic backgrounds. In this review, we provide basic knowledge pyroptosis, explain tumors, focus on significance tumor treatment. addition, further summarize possibility as a potential treatment strategy describe side effects radiotherapy chemotherapy caused by pyroptosis. brief, double-edged sword for rational use dual effect will help us explore formation ideas patients to develop new drugs based

Language: Английский

Citations

1568

Molecular mechanisms and functions of pyroptosis, inflammatory caspases and inflammasomes in infectious diseases DOI
Si Ming Man, Rajendra Karki, Thirumala‐Devi Kanneganti

et al.

Immunological Reviews, Journal Year: 2017, Volume and Issue: 277(1), P. 61 - 75

Published: April 30, 2017

Summary Cell death is a fundamental biological phenomenon that essential for the survival and development of an organism. Emerging evidence also indicates cell contributes to immune defense against infectious diseases. Pyroptosis form inflammatory programmed pathway activated by human mouse caspase‐1, caspase‐4 caspase‐5, or caspase‐11. These caspases are used host control bacterial, viral, fungal, protozoan pathogens. requires cleavage activation pore‐forming effector protein gasdermin D caspases. Physical rupture causes release pro‐inflammatory cytokines IL ‐1β ‐18, alarmins endogenous danger‐associated molecular patterns, signifying potential pyroptosis. Here, we describe central role pyroptosis in mediating immunity infection clearance

Language: Английский

Citations

1369

Necroptosis, pyroptosis and apoptosis: an intricate game of cell death DOI Creative Commons
Damien Bertheloot, Eicke Latz, Bernardo S. Franklin

et al.

Cellular and Molecular Immunology, Journal Year: 2021, Volume and Issue: 18(5), P. 1106 - 1121

Published: March 30, 2021

Abstract Cell death is a fundamental physiological process in all living organisms. Its roles extend from embryonic development, organ maintenance, and aging to the coordination of immune responses autoimmunity. In recent years, our understanding mechanisms orchestrating cellular its consequences on immunity homeostasis has increased substantially. Different modalities what become known as ‘programmed cell death’ have been described, some key players these processes identified. We learned more about intricacies that fine tune activity common ultimately shape different types death. These studies highlighted complex tipping balance between fates. Here, we summarize latest discoveries three most well understood death, namely, apoptosis, necroptosis, pyroptosis, highlighting unique pathways their effect surrounding cells organism whole.

Language: Английский

Citations

1367

Synergism of TNF-α and IFN-γ Triggers Inflammatory Cell Death, Tissue Damage, and Mortality in SARS-CoV-2 Infection and Cytokine Shock Syndromes DOI Creative Commons
Rajendra Karki, Bhesh Raj Sharma, Shraddha Tuladhar

et al.

Cell, Journal Year: 2020, Volume and Issue: 184(1), P. 149 - 168.e17

Published: Nov. 18, 2020

Language: Английский

Citations

1282

Cleavage of DFNA5 by caspase-3 during apoptosis mediates progression to secondary necrotic/pyroptotic cell death DOI Creative Commons

Corey Rogers,

Teresa Fernandes‐Alnemri,

Lindsey Mayes

et al.

Nature Communications, Journal Year: 2017, Volume and Issue: 8(1)

Published: Jan. 3, 2017

Abstract Apoptosis is a genetically regulated cell suicide programme mediated by activation of the effector caspases 3, 6 and 7. If apoptotic cells are not scavenged, they progress to lytic inflammatory phase called secondary necrosis. The mechanism which this occurs unknown. Here we show that caspase-3 cleaves GSDMD-related protein DFNA5 after Asp270 generate necrotic DFNA5-N fragment targets plasma membrane induce necrosis/pyroptosis. Cells express necrosis, when stimulated with triggers such as etoposide or vesicular stomatitis virus infection, but disassemble into small bodies deleted. Our findings identify central molecule regulates disassembly progression provide molecular for Because DFNA5-induced necrosis GSDMD-induced pyroptosis dependent on caspase activation, propose forms programmed

Language: Английский

Citations

1232

The gasdermins, a protein family executing cell death and inflammation DOI
Petr Brož, Pablo Pelegrı́n, Feng Shao

et al.

Nature reviews. Immunology, Journal Year: 2019, Volume and Issue: 20(3), P. 143 - 157

Published: Nov. 5, 2019

Language: Английский

Citations

1230

Gasdermins: Effectors of Pyroptosis DOI

Stephen B. Kovacs,

Edward A. Miao

Trends in Cell Biology, Journal Year: 2017, Volume and Issue: 27(9), P. 673 - 684

Published: June 13, 2017

Language: Английский

Citations

1106