Abstract
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) D2 is the major prostanoid secreted from the activated mast cell and has long been implicated in allergic diseases. The involvement of PGD2 in allergic inflammation has been corroborated by several studies. Two PGD2 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 PGD2-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 PGD2 secreted from activated mast cells may be involved in the formation and/or maintenance of allergic inflammations through its dual receptor systems.
