Advanced search
1 file | 1.22 MB Add to list

Necroptosis: the release of damage-associated molecular patterns and its physiological relevance

Agnieszka Kaczmarek (UGent) , Peter Vandenabeele (UGent) and Dmitri Krysko (UGent)
(2013) IMMUNITY. 38(2). p.209-223
Author
Organization
Abstract
Regulated necrosis, termed necroptosis, is negatively regulated by caspase-8 and is dependent on the kinase activity of RIPK1 and RIPK3. Necroptosis leads to rapid plasma membrane permeabilization and to the release of cell contents and exposure of damage-associated molecular patterns (DAMPs). We are only beginning to identify the necroptotic DAMPs, their modifications, and their potential role in the regulation of inflammation. In this review, we discuss the physiological relevance of necroptosis and its role in the modulation of inflammation. For example, during viral infection, RIPK3-mediated necroptosis acts as a backup mechanism to clear pathogens. Necroptosis is also involved in apparently immunologically silent maintenance of T cell homeostasis. In contrast, the induction of necroptosis in skin, intestine, systemic inflammatory response syndrome, and ischemia reperfusion injury provoke a strong inflammatory response, which might be triggered by emission of DAMPs from necroptotic cells, showing the detrimental side of necroptosis.
Keywords
RECEPTOR-INTERACTING PROTEIN, TUMOR-NECROSIS-FACTOR, ISCHEMIA-REPERFUSION INJURY, INDEPENDENT CELL-DEATH, GROUP BOX 1, NECROTIC CELLS, PROGRAMMED NECROSIS, INFLAMMATORY RESPONSE, APOPTOTIC CELLS, DENDRITIC CELLS

Downloads

  • (...).pdf
    • full text
    • |
    • UGent only
    • |
    • PDF
    • |
    • 1.22 MB

Citation

Please use this url to cite or link to this publication:

MLA
Kaczmarek, Agnieszka, Peter Vandenabeele, and Dmitri Krysko. “Necroptosis: The Release of Damage-associated Molecular Patterns and Its Physiological Relevance.” IMMUNITY 38.2 (2013): 209–223. Print.
APA
Kaczmarek, Agnieszka, Vandenabeele, P., & Krysko, D. (2013). Necroptosis: the release of damage-associated molecular patterns and its physiological relevance. IMMUNITY, 38(2), 209–223.
Chicago author-date
Kaczmarek, Agnieszka, Peter Vandenabeele, and Dmitri Krysko. 2013. “Necroptosis: The Release of Damage-associated Molecular Patterns and Its Physiological Relevance.” Immunity 38 (2): 209–223.
Chicago author-date (all authors)
Kaczmarek, Agnieszka, Peter Vandenabeele, and Dmitri Krysko. 2013. “Necroptosis: The Release of Damage-associated Molecular Patterns and Its Physiological Relevance.” Immunity 38 (2): 209–223.
Vancouver
1.
Kaczmarek A, Vandenabeele P, Krysko D. Necroptosis: the release of damage-associated molecular patterns and its physiological relevance. IMMUNITY. 2013;38(2):209–23.
IEEE
[1]
A. Kaczmarek, P. Vandenabeele, and D. Krysko, “Necroptosis: the release of damage-associated molecular patterns and its physiological relevance,” IMMUNITY, vol. 38, no. 2, pp. 209–223, 2013.
@article{3148387,
  abstract     = {Regulated necrosis, termed necroptosis, is negatively regulated by caspase-8 and is dependent on the kinase activity of RIPK1 and RIPK3. Necroptosis leads to rapid plasma membrane permeabilization and to the release of cell contents and exposure of damage-associated molecular patterns (DAMPs). We are only beginning to identify the necroptotic DAMPs, their modifications, and their potential role in the regulation of inflammation. In this review, we discuss the physiological relevance of necroptosis and its role in the modulation of inflammation. For example, during viral infection, RIPK3-mediated necroptosis acts as a backup mechanism to clear pathogens. Necroptosis is also involved in apparently immunologically silent maintenance of T cell homeostasis. In contrast, the induction of necroptosis in skin, intestine, systemic inflammatory response syndrome, and ischemia reperfusion injury provoke a strong inflammatory response, which might be triggered by emission of DAMPs from necroptotic cells, showing the detrimental side of necroptosis.},
  author       = {Kaczmarek, Agnieszka and Vandenabeele, Peter and Krysko, Dmitri},
  issn         = {1074-7613},
  journal      = {IMMUNITY},
  keywords     = {RECEPTOR-INTERACTING PROTEIN,TUMOR-NECROSIS-FACTOR,ISCHEMIA-REPERFUSION INJURY,INDEPENDENT CELL-DEATH,GROUP BOX 1,NECROTIC CELLS,PROGRAMMED NECROSIS,INFLAMMATORY RESPONSE,APOPTOTIC CELLS,DENDRITIC CELLS},
  language     = {eng},
  number       = {2},
  pages        = {209--223},
  title        = {Necroptosis: the release of damage-associated molecular patterns and its physiological relevance},
  url          = {http://dx.doi.org/10.1016/j.immuni.2013.02.003},
  volume       = {38},
  year         = {2013},
}

Altmetric
View in Altmetric
Web of Science
Times cited: