The IL-1-like cytokine IL-33 is inactivated after maturation by caspase-1

By C. Cayrol, J. Girard. Proceedings of the National Academy of Sciences of the United States of America, 2009

740 citations recorded by the source corpus.

Subfields: Immunology, Surgery

View Paper: https://www.semanticscholar.org/paper/bdefd181b8d650f3a0bbf00bb005889633722f0c

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. J. Girard
2. C. Cayrol
3. F. Liew
4. G. Núñez
5. Grace Y. Chen
6. Andrew N. J. McKenzie
7. I. McInnes
8. D. Umetsu

In Surgery

1. C. Cayrol
2. J. Girard
3. F. Liew
4. G. Núñez
5. Andrew N. J. McKenzie
6. D. Umetsu
7. R. DeKruyff
8. C. A. Dinarello

Citations in the corpus

• THE INTERLEUKIN-1 FAMILY: BACK TO THE FUTURE (2013, neutral): “IL-33 is inactivated by caspase-1 (Cayrol and Girard, 2009), and the 30 KDa protein is one of its bioactive forms.”
• Sterile inflammation: sensing and reacting to damage (2010, background): “Extracellular IL-33 that is released during necrosis also functions as an alarmin to alert cells, such as mast cells and other innate immune cells, to tissue damag”
• The Impact of Oxidative Stress and Inflammation on RPE Degeneration in Non-neovascular AMD (2017, background): “C3a, C5a, and C5b-9 complexes are implicated in activating the inflammasome, composed of NLRP3, ASP, and Pro-caspase1, which upon activation, is cleaved to convert pro-IL-1β, pro-IL-18, and pro-IL-33 into their active forms.”
• Disease-associated functions of IL-33: the new kid in the IL-1 family (2010, background): “Full-length IL-33 is biologically active and this activity is mediated by the IL-1-like domain at the carboxyl terminu”
• IL-33 is a crucial amplifier of innate rather than acquired immunity (2010, background): “Like pro-IL-1α, pro-IL-33, but not caspasecleaved IL-33 (23–25), has biological activity and is suggested to act as an alarmin, an endogenous danger signal that alerts immune cells, in necrosis-, rather than apoptosis-, associated tissue injury during trauma and/or infection (23, 24).”
• Innate lymphoid cells mediate influenza-induced airway hyper-reactivity independently of adaptive immunity (2011, background): “However, IL-33 may not require caspase-1-mediated proteolysis for activatio”
• The IL-1 family: regulators of immunity (2010, background): “IL-33 has subsequently been shown not to be processed into the mature active cytokine by caspase 1, but to be inactivated by its cleavage in the cytokine domain by caspase 1 or caspase 3 (Ref”
• IL-33: an alarmin cytokine with crucial roles in innate immunity, inflammation and allergy. (2014, background): “Inactivation of IL-33 during apoptosis is likely to be important to avoid alerting the immune system unnecessarily after physiological programmed (apoptotic) cell death, as opposed to pathological (necrotic) cell death [45,46].”