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- W4386258231 abstract "Apoptosis is traditionally considered to be an immunologically silent form of cell death. Multiple mechanisms exist to ensure that apoptosis does not stimulate the immune system to cause inflammation or autoimmunity. Against this expectation, we now report that epithelia are programmed to provoke, rather than suppress, inflammation in response to apoptosis. We found that an acute inflammatory response led by neutrophils occurs in zebrafish and cell culture when apoptotic epithelial cells cannot be expelled from the monolayer by apical extrusion. This reflects an intrinsic circuit where ATP released from apoptotic cells stimulates epithelial cells in the immediate vicinity to produce interleukin-8 (IL-8). Apical extrusion therefore prevents inappropriate epithelial inflammation by physically eliminating apoptotic cells before they can activate this pro-inflammatory circuit. This carries the implication that epithelia may be predisposed to inflammation, elicited by sporadic or induced apoptosis, if apical extrusion is compromised." @default.
- W4386258231 created "2023-08-30" @default.
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- W4386258231 date "2023-08-01" @default.
- W4386258231 modified "2023-10-02" @default.
- W4386258231 title "Apical extrusion prevents apoptosis from activating an acute inflammatory program in epithelia" @default.
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- W4386258231 doi "https://doi.org/10.1016/j.devcel.2023.08.009" @default.
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