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. 2018 May 4;9:832. doi: 10.3389/fimmu.2018.00832

Figure 3.

Figure 3

P2Y2R and P2X7R signaling during injury and inflammation. Adenosine triphosphate (ATP) can be released by necrotic cells or apoptotic cells though cytoplasmic channel, pannexin 1. When engaging P2Y2R, released ATP functions as “find me signal” for macrophages phagocytosis of injured cells and promotes so wound healing. P2Y2R signaling contributes also to bacterial clearance by stimulating neutrophils chemotaxis. However, excess P2Y2R signaling in neutrophils or eosinophils contributes, respectively, to chronic lung inflammation and allergic airway disease by promoting the release of pro-allergic mediators. P2X7R signaling promotes the killing of intracellular bacteria such as Mycobacter Tuberculosis. In dendritic cells, P2X7R signaling promotes T-cell priming which has been implicated in allergic diseases, graft-versus-host disease (GVH) as well as in psoriasis and inflammatory bowel disease.