Suppression of interleukin-33 bioactivity through proteolysis by apoptotic caspases.

By A. Lüthi, Sean P. Cullen, E. McNeela, P. Duriez, Inna S. Afonina, Clare Sheridan, G. Brumatti, Rebecca C. Taylor, K. Kersse, Peter Vandenabeele and 2 more. Immunity, 2009

716 citations recorded by the source corpus.

Subfields: Immunology, Surgery

View Paper: https://www.semanticscholar.org/paper/1679ae04d14ac7d73c76352f9a10922117670c77

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. C. Cayrol
2. J. Girard
3. J. Allen
4. Rick M. Maizels
5. Yan Yu
6. Weitong Gao
7. Yang Zhou
8. Xuepeng Wang

In Surgery

1. C. Cayrol
2. J. Girard

Citations in the corpus

• Pattern Recognition Receptors and the Host Cell Death Molecular Machinery (2018, background): “Indeed the apoptotic process reduce cell immunogenicity by diverse ways including, (1) preservation of intracellular structures and plasma membrane, thereby blocking the release of DAMPS; (2) reduction of cellular volume, by condensation of the nucleus and shedding of small vesicles, which favors it”
• Autophagy, ferroptosis, pyroptosis, and necroptosis in tumor immunotherapy (2022, background): “as immunomodulatory cytokines have been attributed to either initiate adaptive antitumor responses or inhibit antitumor immune effects depending on the makeup of cytokine milieu.(269,323) Furthermore, Liu’s study found that CAR-T cells could promote GSDME-mediated tumor cell pyroptosis by releasing ”
• Diversity and dialogue in immunity to helminths (2011, background): “For example, functionally active IL-33, another potent inducer of T H 2-type cytokines, is released from the nucleus following necrotic but not apoptotic cell death of fibroblasts, endothelial cells and epithelial cell”
• 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].”
• 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).”