The role of prostaglandin E2 receptor signaling of dendritic cells in rheumatoid arthritis

• PGE2 has different and sometimes opposite effects on DC function.
• Targeting EP2/4 receptor signaling may be a mechanism for regulating DC function.
• Understanding the effects of PGE2-EP on DC in RA will find new therapeutic targets.
• Facilitate the development of therapeutics for RA by interfering with EP4 and DC.

Prostaglandin E2 (PGE2), a very potent lipid mediator produced from arachidonic acid (AA) through the action of cyclooxygenase (COX) enzymes, is implicated in the regulation of dendritic cell (DC) functions such as differentiation ability, cytokine-producing capacity, Th-cell polarizing ability, migration and maturation. DCs are the most potent antigen-presenting cells and play major roles in both the induction of primary immune responses and tolerance. It is well established that PGE2 functions significantly in the pathogenesis of rheumatoid arthritis (RA). Although the role of PGE2 in RA has been studied extensively, the effects of PGE2 on DC biology and the role of DCs in RA have not become the focus of investigation until recently. Here, we summarize the latest progress in PGE2 research with respect to DC functions, as well as the role of PGE2 receptor signaling of DCs in the pathogenesis of RA.