Allergic
inflammations feature an accumulation of T helper 2 (Th2) cells, eosinophils, and basophils into the inflamed sites and are often triggered by
antigen-
IgE mediated activation of mast cells that secret a variety of mediators. Therefore, the mast cell is known as a conductor cell in allergic
inflammations.
Prostaglandin (PG) D(2) is the major
prostanoid secreted from the activated mast cell and has long been implicated in allergic diseases. The involvement of
PGD(2) in allergic
inflammation has been corroborated by several studies. Two
PGD(2) receptors are known as the DP receptor and CRTH2. CRTH2 differs from DP in its signal pathways: CRTH2 is coupled with Gi-type
G protein and DP is coupled with Gs-type
G protein. It was reported that DP-deficient mice subjected to
ovalbumin-induced
asthma model systems showed suppressed
allergic reactions. Functions of CRTH2 in vivo have not been clear, but CRTH2 mediates PGD(2)-dependent cell migration and the activation of Th2 cells, eosinophils, and basophils. Therefore, the CRTH2 signal seems to promote allergic disease. The findings from these in vivo and vitro studies suggest that
PGD(2) secreted from activated mast cells may be involved in the formation and/or maintenance of allergic
inflammations through its dual receptor systems.