Identification of a key pathway required for the sterile inflammatory response triggered by dying cells

By Chun-jen Chen, H. Kono, D. Golenbock, G. Reed, Shizuo Akira, K. Rock. Nature Medicine, 2007

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Cancer-related inflammation, the seventh hallmark of cancer: links to genetic instability. (2009, background): “secreted, can be poured out from necrotizing cells and serve as a “danger signal” for mounting antitumor immunity [54].”
THE INTERLEUKIN-1 FAMILY: BACK TO THE FUTURE (2013, neutral): “and colitis, reduced atherosclerosis (Chen et al., 2007; Krelin et al., 2007)”
The IL-1-like cytokine IL-33 is inactivated after maturation by caspase-1 (2009, background): “Another property of IL-33 that qualifies it as a bona fide danger signal is the fact IL-33 signals through the TLR/IL-1R/MyD88 signaling pathway (4, 13, 17), like IL-1 (27) and the exogenous danger signals from microorganisms, the so-called pathogen-associated molecular patterns.”
Apoptosis: controlled demolition at the cellular level (2008, background): “Necrotic cells almost invariably trigger inflammation by neutrophils, macrophages and other cells of the innate immune system, and recent evidence suggests that this is caused by the release of molecules (collectively called danger-associated molecular patterns (DAMPs) or alarmins) that stimulate on”