Figure 5
Figure 5. NF157, but not P2X1R, specific antagonists MRS2159 and NF023 restore NK responsiveness to CX3CL1. (A) NK-cell chemotaxis to 10 ng/mL CX3CL1 in the presence or absence of 100μM ATP with or without 30-minute pretreatment with 100μM NF157, 10μM MRS2159, or 1μM NF023. *P < .05, CX3CL1 versus CX3CL1 + ATP. (B) NK-cell killing of HUVECs after stimulation with or without 10 ng/mL CX3CL1 in the presence or absence of ATP and the indicated inhibitors. *P < .05, CX3CL1 versus CX3CL1 + ATP. (C) Chemotaxis of NK cells to CX3CL1 with or without ATP and in the presence or absence of phenol red. *P < .05, CX3CL1 versus CX3CL1 + ATP. (D) NK-cell killing of HUVECs stimulated or not with CX3CL1 with or without ATP and the presence or absence of phenol red. *P < .05, CX3CL1 versus CX3CL1 + ATP.

NF157, but not P2X1R, specific antagonists MRS2159 and NF023 restore NK responsiveness to CX3CL1. (A) NK-cell chemotaxis to 10 ng/mL CX3CL1 in the presence or absence of 100μM ATP with or without 30-minute pretreatment with 100μM NF157, 10μM MRS2159, or 1μM NF023. *P < .05, CX3CL1 versus CX3CL1 + ATP. (B) NK-cell killing of HUVECs after stimulation with or without 10 ng/mL CX3CL1 in the presence or absence of ATP and the indicated inhibitors. *P < .05, CX3CL1 versus CX3CL1 + ATP. (C) Chemotaxis of NK cells to CX3CL1 with or without ATP and in the presence or absence of phenol red. *P < .05, CX3CL1 versus CX3CL1 + ATP. (D) NK-cell killing of HUVECs stimulated or not with CX3CL1 with or without ATP and the presence or absence of phenol red. *P < .05, CX3CL1 versus CX3CL1 + ATP.

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