Figure 3.
Figure 3. ATP inhibits DC migration through activation of P2R. (A) Nucleotides with specific binding affinities to P2R were tested at various concentrations for their ability to inhibit the migration of MoDCs, matured with TNF-α, IFN-α, and PGE2 for 24 hours, to CCL21. (B) Effect of nucleotides (at 100 μM) on the migration of migratory-type MoDCs to CCL21. Migration in the absence of nucleotides was normalized to 100% (mean ± SEM; n ≥ 5). (C) Effect of P2R antagonists on the inhibitory effect of ATP (100 μM) on MoDC migration. Migratory-type MoDCs were incubated with 30 μM suramin, 100 μM reactive blue-2 (RB-2), 100 μM PPADS, or 300 μM oxidized ATP (oxiATP) 45 minutes before the assessment of migration (mean ± SEM; n = 5-8). *P < .01. (D) Effect of P2R agonists (at 100 μM) on the migration of CD1a+ dermal DCs toward CCL21.

ATP inhibits DC migration through activation of P2R. (A) Nucleotides with specific binding affinities to P2R were tested at various concentrations for their ability to inhibit the migration of MoDCs, matured with TNF-α, IFN-α, and PGE2 for 24 hours, to CCL21. (B) Effect of nucleotides (at 100 μM) on the migration of migratory-type MoDCs to CCL21. Migration in the absence of nucleotides was normalized to 100% (mean ± SEM; n ≥ 5). (C) Effect of P2R antagonists on the inhibitory effect of ATP (100 μM) on MoDC migration. Migratory-type MoDCs were incubated with 30 μM suramin, 100 μM reactive blue-2 (RB-2), 100 μM PPADS, or 300 μM oxidized ATP (oxiATP) 45 minutes before the assessment of migration (mean ± SEM; n = 5-8). *P < .01. (D) Effect of P2R agonists (at 100 μM) on the migration of CD1a+ dermal DCs toward CCL21.

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