Autophagy is an intracellular degradation system by which cytoplasmic contents are degraded in lysosomes. In response to nutrient depletion, phagophores are generated, which sequester a portion of the cytoplasm, forming autophagosomes, which ultimately fuse with lysosomes to re-utilize the digested contents. Numerous studies have shown that such a conventional mode of autophagic flux may play a critical role in both physiological and disease processes. However, it is possible that a different mode of autophagic flux exists. In a recent publication in J Immunol (Takenouchi et al, 2009, 182:2051-62), we observed that activation of the purinergic P2X7 receptor (P2X7R) by ATP treatment in microglial cells resulted in the release of autolysosomes into the extracellular space, providing a novel mechanism for the clearance of intracellular pathogens during the course of inflammation. Furthermore, given the role of the P2X7R signaling pathway in inflammation and neurodegeneration, this non-canonical autophagic pathway might explain the mechanism of the release of various cytoplasmic proteins, such as interleukin-1β and α-synuclein.
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Takenouchi et al. (2009) studied this question.