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Article Addendum
Phagocytosis of Cells Dying through Autophagy Evokes a Pro-Inflammatory Response in Macrophages
Goran Petrovski, Gábor Zahuczky, Gyöngyike Májai and László Fésüs
volume 3 | issue 5
September/October 2007Pages: 508 - 510
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Autophagy as a natural part of cellular homeostasis usually takes place unnoticed by neighboring cells. However, its co-occurrence with cell death may contribute to the clearance of these dying cells by recruited phagocytes. Autophagy associated with programmed cell death has recently been reported to be essential for presentation of phoshatidylserine (PS) on the cell surface (Qu et al. 2007) that has a key role in the clearance of apoptotic cells. Recently, we have demonstrated that upon triggering cell death by autophagy in MCF-7 cells, the corpses were efficiently phagocytosed by both human macrophages and non-dying MCF-7 cells. Death as well as engulfment could be prevented by inhibiting autophagy. Based on our data, two molecular mechanisms have been proposed for the uptake of cells which die through autophagy: a PS-dependent pathway which was exclusively used by the living MCF-7 cells acting as non-professional phagocytes, and a PS-independent uptake mechanism that was active in macrophages acting as professional phagocytes. Several lines of evidence suggest that macrophages utilize calreticulin-mediated recognition, tethering, tickling and engulfment processes. Phagocytic uptake of cells dying through autophagy by macrophages leads to a pro-inflammatory response characterized by the induction and secretion of IL-6, TNFα, IL-8 and IL-10.
Addendum to:
Clearance of Dying Autophagic Cells of Different Origin
by Professional and Non-Professional Phagocytes
G. Petrovski, G. Zahuczky, K. Katona, G. Vereb, W. Martinet, Z. Nemes, W. Bursch and L. Fésüs
Cell Death Differ 2007;14:1117-28
Authors
Goran Petrovski
University of Debrecen
Gábor Zahuczky
University of Debrecen
Gyöngyike Májai
University of Debrecen
László Fésüs
University of Debrecen
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.