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IL-1α responds to necrotic cell death

Nature Medicine volume 13, pages 778–780 (2007)Cite this article

Necrosis induces inflammation, but how necrotic cells signal to immune cells was poorly understood. New work by Chen et al. shows that IL-1α acts as a mediator, translating a signal from the necrotic cells to induce the recruitment of immune cells to the site of injury (pages 851–856).

Death used to be simple — end of story. For much of medical science these days, cell death begins a narrative with many different endings. Widespread cell death kills, but after a sublethal insult, the precise mode of cell death will determine the outcome. Cells die in three different ways — apoptosis, autophagy or necrosis — that can be distinguished by cell morphology and the biochemical pathways that are, or are not, initiated1. Necrosis was described first and has the most dramatic outcome, invariably leading to an inflammatory immune response. Considering that it potentially has the most serious consequences, it is surprising that necrosis has been studied less intensely than apoptosis or autophagy, especially as biochemical programs (for example, activation of phospholipases and of poly-ADP-ribose polymerase) triggered in response to necrosis are increasingly being recognized2. In this issue, Chen et al.3 help to redress this imbalance by identifying interleukin (IL)-1α as a key mediator of the acute inflammatory response to necrotic cells.

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Figure 1: Necrotic cells stimulate neutrophilic inflammation through IL-1α.

Katie Ris

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Authors and Affiliations

  1. Keith B. Elkon is in the Departments of Medicine and Immunology, University of Washington, 1959 NE Pacific Avenue, Box 356428, Seattle, Washington 98195, USA. elkon@u.washington.edu,

    Keith B Elkon

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Elkon, K. IL-1α responds to necrotic cell death. Nat Med 13, 778–780 (2007). https://doi.org/10.1038/nm0707-778

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