Figure 4
Figure 4. Different outcomes of immune cells exposed to eATP. Depending on the P2 receptor subtype expressed, the concentration in the extracellular milieu, and the duration of stimulation, eATP may induce pro- or anti-inflammatory responses. Millimolar concentrations of eATP open the P2X7 channel. Whereas the opening of the P2X7 channel for a short period of time leads to the activation of a number of mechanisms that sustain inflammation, prolonged stimulation of the P2X7 channel induces apoptosis of cells and consequent immune suppression. Relatively low (micromolar) concentrations of eATP activate the high-affinity receptor P2Y11, which is coupled to a Gs protein and induces an increase in intracellular concentration of cAMP, a well-known negative regulator of immune cells. Engagement of P2Y11 inhibits several effector mechanisms, including NK- and T-cell proliferation, cytokine production, and cytotoxic activity, thus contributing to the resolving phase of inflammation. In this model, ATP would act both as an initiator and terminator of immune response.

Different outcomes of immune cells exposed to eATP. Depending on the P2 receptor subtype expressed, the concentration in the extracellular milieu, and the duration of stimulation, eATP may induce pro- or anti-inflammatory responses. Millimolar concentrations of eATP open the P2X7 channel. Whereas the opening of the P2X7 channel for a short period of time leads to the activation of a number of mechanisms that sustain inflammation, prolonged stimulation of the P2X7 channel induces apoptosis of cells and consequent immune suppression. Relatively low (micromolar) concentrations of eATP activate the high-affinity receptor P2Y11, which is coupled to a Gs protein and induces an increase in intracellular concentration of cAMP, a well-known negative regulator of immune cells. Engagement of P2Y11 inhibits several effector mechanisms, including NK- and T-cell proliferation, cytokine production, and cytotoxic activity, thus contributing to the resolving phase of inflammation. In this model, ATP would act both as an initiator and terminator of immune response.

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