Abstract
SummaryMacrophages are multifunctional cells that perform diverse roles in health and disease. Emerging evidence has suggested that these innate immune cells might also be capable of developing immunological memory, a trait previously associated with the adaptive system alone. While recent studies have focused on the dramatic macrophage reprogramming that follows infection and protects against secondary microbial attack, can macrophages also develop memory in response to other cues? Here, we show that apoptotic corpse engulfment by Drosophila macrophages is an essential primer for their inflammatory response to tissue damage and infection in vivo. Priming is triggered via calcium-induced JNK signaling, which leads to upregulation of the damage receptor Draper, thus providing a molecular memory that allows the cell to rapidly respond to subsequent injury or infection. This remarkable plasticity and capacity for memory places macrophages as key therapeutic targets for treatment of inflammatory disorders.
Highlights
The innate immune system has been distinguished from the adaptive system by its marked lack of immunological memory (Roitt et al, 2006)
Macrophages and natural killer (NK) cells have emerged as the main innate immune cells responsible for this priming phenomenon and appear to undergo a profound phenotypic reprogramming upon exposure to microbial stimuli that changes their response to secondary infection (Bowdish et al, 2007)
We find that 100% of calcium flashes are accompanied by corpse uptake
Summary
Macrophages that consume apoptotic corpses during fly development become primed for inflammatory responses later in life, establishing a form of molecular memory that aids in the response to bacterial infection and tissue damage.
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