How dying cells alert the immune system to danger
By H. Kono, K. Rock. Nature reviews. Immunology, 2008
1,803 citations recorded by the source corpus.
When a cell dies in vivo, the event does not go unnoticed. The host has evolved mechanisms to detect the death of cells and rapidly investigate the nature of their demise. If cell death is a result of natural causes — that is, it is part of normal physiological processes — then there is little threat to the organism. In this situation, little else is done other than to remove the corpse. However, if cells have died as the consequence of some violence or disease, then both defence and repair mechanisms are mobilized in the host. The importance of these processes to host defence and disease pathogenesis has only been appreciated relatively recently. This article reviews our current knowledge of these processes.
Subfields: Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/5ef97acdc2c8a3eaf13d32f14efa1d053f4d07bf
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Citations in the corpus
- Mechanisms of Cisplatin Nephrotoxicity (2010, background): “endogenous molecules, termed “alarmins” or damage-associated molecular pattern molecules (DAMPs), associated with tissue injury [166].”
- Phagocyte partnership during the onset and resolution of inflammation (2010, background): “For example, in contrast to cells undergoing apoptosis, necrotic cell death resulting from infection or injury leads to the disruption of cell membranes and the release of cytoplasmic and nuclear component”
- The immunology of stroke: from mechanisms to translation (2011, background): “Dying and dead cells release 'danger signals' that activate the immune syste”
- Mitochondria in innate immune responses (2011, background): “Mitochondria and cellular damage responses In addition to recognizing a diverse array of microbial PAMPs, it is now well appreciated that PRRs of the innate immune system sense cellular damage and stress in the absence of microbial infectio”
- Para-inflammation in the aging retina. (2009, background): “By contrast, during apoptotic cell death, the integrity of cell membrane is not disrupted initially and the DAMP molecules are contained within the apoptotic cells (Bianchi and Manfredi, 2007; Kono and Rock, 2008; Rock and Kono, 2008).”
- Sterile inflammation: sensing and reacting to damage (2010, background): “DAMPs have been identified by their ability to induce inflammatory responses in vitro and/or in vivo when purified and by the observed reduction in inflammation when they are selectively deplete”
- Recent advances in 2D and 3D in vitro systems using primary hepatocytes, alternative hepatocyte sources and non-parenchymal liver cells and their use in investigating mechanisms of hepatotoxicity, cell signaling and ADME (2013, neutral): “Thus, it is very likely that this early necrotic cells trigger an inflammatory response (Kono and Rock 2008).”
- The inflammasomes: guardians of the body. (2009, background): “This led to multiple studies identifying molecules and signals that are released by damaged or stressed tissues and that trigger or modulate the immune response (88, 89).”
- Necrotic cells trigger a sterile inflammatory response through the Nlrp3 inflammasome (2009, background): “S terile inflammatory insults such as trauma or ischemia trigger a robust influx of neutrophils and monocytes to the site of tissue injury (1).”
- Phosphorylation-Driven Assembly of RIP1-RIP3 Complex Regulates Programmed Necrosis and Virus-Induced Inflammation (2009, positive): “The release of endogenous ‘‘danger signals’’ from necrotic cells induces inflammation and can activate immune responses, trigger inflammatory diseases, and promote cancer growth (Kono and Rock, 2008).”
- Host type I IFN signals are required for antitumor CD8+ T cell responses through CD8α+ dendritic cells (2011, background): “Recently, it has been shown that dsDNA can be released from necrotic cells, reach the cytoplasm of APCs, and be recognized by a TLR-independent on January 17, 2012 jem .rupress.org D ow nloaded from JEM Vol. 208, No. 10 Article 2013 of type I IFNs, which are already FDA approved for other indication”
- Toll-like receptor activation of XBP1 regulates innate immune responses in macrophages (2010, background): “Microbial products are not the only signals that modulate innate immune responses, as signals produced by stressed or damaged tissues have also been suggested to modulate the inflammatory respons”
- The Biology of Regeneration Failure and Success After Spinal Cord Injury. (2018, background): “In contrast, apoptosis is an ordered, ATP-driven process of cell death marked by tightly packed condensation of the cell body that elicits a far less potent inflammatory signal than necrosis (FIGURE 2E) (209).”