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In every case, the AA genotype was associated with a higher percentage of CRTh2-expressing cells compared to the GG genotype, with a mean difference of 1.7-fold (P?ALK did not reach significance (Fig.?3B). These data suggest the AA genotype influences the propensity of CD4+ T cells to undergo Th2 differentiation. To study whether rs533116 was associated with enhanced receptor function, CRTh2+ Th2 cells with the AA or GG genotype were stimulated with the CRTh2-specific agonist, DK-PGD2. Cells with the AA genotype demonstrated ~ 2-fold higher percentage of cells expressing IL-4 and IL-13 compared to cells with the GG genotype (P?VEGFR inhibitor is associated with both allergic asthma and expression of CRTh2. It also provides the first comprehensive this website characterization of the proportion of circulating cells expressing CRTh2, demonstrating increases in CRTh2-expressing eosinophils, basophils and CD4+ T cells. Furthermore, we observed that virtually all CCR3+ eosinophils express CRTh2, which may reflect synergy between these chemotactic pathways. PGD2 has been shown to enhance eotaxin-induced eosinophil release from the bone marrow and to maintain activity in blood, suggesting a role in mediating tissue infiltration [24, 25]. The higher percentage of CRTh2+CD4+ T cells is in line with a recent study showing that allergen-specific CD4+ T cells expressing CRTh2 are increased in blood of allergic compared to nonallergic subjects [26]. In contrast, Mutalithas et?al. showed no increase in blood CD3+CRTh2+ cells in asthmatics compared to nonasthmatics, although they did not control for atopy [15]. Collectively, these studies indicate that the increases in CRTh2-expressing cells observed within tissues of allergic subjects may be due, at least in part, to infiltration of circulating cells. This study shows a significant association between CRTh2 rs533116 and allergic asthma among White adults, those demonstrating the highest frequency of the AA genotype.