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The anti-inflammatory effect of apoptotic bodies

The ubiquitous process of apoptotic cell death escaped the notice of cell biologists for decades, largely because cells that die by this mechanism are efficiently removed by phagocytosis in a process that provokes no local inflammation. Indeed, as Henson and collaborators have argued, the clearance of apoptotic debris is not merely silent, but actually suppresses inflammation. These authors previously identified a major phagocytic receptor for apoptotic cells, the phosphatidylserine (PS) receptor (PSR), which binds a phospholipid that is usually restricted to the inner leaflet of the plasma membrane but that accumulates on the cell surface during apoptosis. Exogenous apoptotic cells introduced into inflamed lung tissue in vivo are taken up by local macrophages, which then release active TGF-b1 and suppress the effects of inflammatory cytokines. Ligation of the PSR appears to be critical for this effect, since instillation of PS vesicles alone confers a similar effect, and live cells?or even apoptotic cells that lack extracellular PS?do not. Crucially, when the apoptotic cells are treated so that they can bind a different phagocytic receptor, the anti-inflammatory effect is also lost, confirming that the interaction with the PSR, rather than phagocytosis per se, helps terminate inflammation in this tissue.


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Contact: John Ashkenas
scied@the-jci.org
416-946-7593
Journal of Clinical Investigation
2-Jan-2002


Page: 1

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