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The impact of the prostaglandin D 2 2 receptor 2 and its downstream effects on the pathophysiology of asthma

机译：前列腺素D 2 2受体2对哮喘病理生理学的影响及其下游影响

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Abstract Current research suggests that the prostaglandin D 2 (PGD 2 ) receptor 2 (DP 2 ) is a principal regulator in the pathophysiology of asthma, because it stimulates and amplifies the inflammatory response in this condition. The DP 2 receptor can be activated by both allergic and nonallergic stimuli, leading to several pro‐inflammatory events, including eosinophil activation and migration, release of the type 2 cytokines interleukin (IL)‐4, IL‐5 and IL‐13 from T helper 2 (Th2) cells and innate lymphoid cells type 2 (ILCs), and increased airway smooth muscle mass via recruitment of mesenchymal progenitors to the airway smooth muscle bundle. Activation of the DP 2 receptor pathway has potential downstream effects on asthma pathophysiology, including on airway epithelial cells, mucus hypersecretion, and airway remodelling, and consequently might impact asthma symptoms and exacerbations. Given the broad distribution of DP 2 receptors on immune and structural cells involved in asthma, this receptor is being explored as a novel therapeutic target.
机译：摘要目前的研究表明，前列腺素D 2（PGD 2）受体2（DP 2）是哮喘病理生理学中的主要调节因子，因为它刺激并放大了这种情况下的炎症反应。可以通过过敏性和非过敏性刺激激活DP 2受体，导致几种促炎事件，包括嗜酸性粒细胞激活和迁移，释放2型细胞因子白细胞介素（IL）-4，IL-5和IL-13来自T.辅助2（TH2）细胞和先天淋巴细胞型2（ILC），并通过募集间充质祖细胞的气道平滑肌肉质量增加到气道平滑肌束。 DP 2受体途径的激活具有对哮喘病理生理学的潜在下游效应，包括气道上皮细胞，粘液过度分泌和呼吸道重塑，因此可能会影响哮喘症状和加剧。鉴于DP 2受体对哮喘涉及哮喘的免疫和结构细胞的广泛分布，该受体正在探索作为一种新的治疗靶标。

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