10 The Korean Journal of Internal Medicine Vol. 26, No. 1, March 2011 Figure 1. TH2 immune response in asthma. Proposed scheme showing TH2 cell immunity in the pathogenesis of bronchial asthma. TH2 cells play an important role, organizing the characteristic inflammatory response, involving mast cells, basophils, and eosinophils. Recent evidence suggests that coordinated expression and cross-regulation between thymic stromal lymphopoietin (TSLP), interleukin (IL)-25, and IL-33 are crucial events for developing TH2 cell-mediated airway immune responses during asthma. These inflammatory cells also produce TH2-type cytokines, indicating that these cells and TH2 cells interact with each other to promote TH2 type inflamma- tion in asthma. activation is a requirement for PGD2 generation in chopped human lung parenchyma [13]. Thus, mast cells are responsible for the bulk of PGD2 production in the allergic setting. PGD2 produced by mast cells may provide an essential link between early-phase and late-phase allergic responses by initiating cellular processes that lead to the recruitment and activation of TH2 cells and eosinophils with associated pathophysiological effects. PGD2-related receptors Among PG receptors, D prostanoid receptor (DP)/DP1, DP2/chemoattractant receptor homologous molecule expressed on TH2 cells (CRTH2), and thromboxane A2 receptor (TP) belong to a family of seven-transmembrane G-protein-coupled receptors (GPCRs), mediating the bio- logical effects of both PGD2 and its metabolites. In con- trast, peroxisome proliferator-activated receptor (PPAR)- γ is a nuclear receptor for PGD2 metabolites. DP, TP, and PPAR-γ are present in various types of hematological and non-hematological cells [14,15]. In contrast, human CRTH2 has been specifically identified on hematological cells [16], although the tissue expression pattern of CRTH2 in humans differs from that in rodents [17]. DP is the most studied PGD2 receptor and its activation leads to Gs-mediated elevation in cAMP. DP is activated by PGD2 and its metabolites, including ∆12-PGD2 and PGJ2. Such activation by DP-selective agonists, such as BW245C, promotes relaxation of both vascular and airway smooth muscle, leading to vasodilatation and bronchodilatation, respectively [18]. DP is also expressed by platelets, in which its activation is linked to an anti-aggregatory func- tion [19]. DP plays both anti-inflammatory and proinflam- matory roles. Accumulation of cAMP is generally associat- ed with the inhibition of effector cell function in lympho- cytes, such as TH1 cells and natural killer cells, and other immune cells, [20]. Consistent with this, DP-mediated signals also suppress cell migration and/or the activation of eosinophils, basophils, netrophils, DCs, and fibroblasts [16,21-24]. Inhalation of a selective DP agonist suppresses