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Department of Biological Sciences, Rutgers University, Newark, NJ 07102
Since dendritic cells (DC) participate in both innate and adaptive immunity, their survival and expansion is tightly controlled. Little is known about the mechanisms of DC apoptosis. PGE2, an arachidonic acid metabolite, plays an essential role in DC migration. We propose a novel function for PGE2 as a DC survival factor. Our studies demonstrate that PGE2 protects DC in vitro against apoptosis induced by withdrawal of growth factors or ceramide. DC matured in conditions that inhibit endogenous PGE2 release are highly susceptible to apoptosis and exogenous PGE2 re-establishes the more resistant phenotype. The antiapoptotic effect is mediated through EP-2/EP-4 receptors and involves the PI3K 
Akt pathway. PGE2 leads to increased phosphorylation of Akt, protection against mitochondrial membrane compromise, and decreased caspase 3 activity. Macroarray data indicate that PGE2 leads to the down-regulation of a number of proapoptotic molecules, i.e., BAD, several caspases, and granzyme B. In vivo, higher numbers of immature and Ag-loaded CFSE-labeled DC are present in the draining lymph nodes of mice inoculated with PGE2 receptor agonists, compared with animals treated with ibuprofen or controls injected with PBS. This suggests that PGE2 acts as an endogenous antiapoptotic factor for DC and raises the possibility of using PGE2 agonists to increase the survival of Ag-loaded DC following in vivo administration.
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