Figure 3
Figure 3. GP1a-treated DCs exhibit lower migratory capacity in vivo. (A) DCs generated from Cnr2+/+ (wt) or Cnr2−/− (ko) mice were treated with CCP with or without GP1a (5μM) for 48 hours and labeled with PKH-26. Then, 1 × 106 labeled DCs were injected subcutaneously in the footpads of wt C57BL/6 mice preinjected with 40 ng of TNF-α s.c in the footpads 24 hours earlier. Recipient mice received CCP-treated DC (control) in the right footpad and CCP + GP1a–treated DCs in the left footpad. Forty-eight hours later, cells were collected from popliteal lymph nodes, and PKH-labeled cells were analyzed by FACS. Data from 3 different experiments are normalized by plotting the number of labeled cells from the control leg as 100%. (B) Supernatants collected from DC cultures before injection were analyzed for MMP-9 via ELISA.

GP1a-treated DCs exhibit lower migratory capacity in vivo. (A) DCs generated from Cnr2+/+ (wt) or Cnr2−/− (ko) mice were treated with CCP with or without GP1a (5μM) for 48 hours and labeled with PKH-26. Then, 1 × 106 labeled DCs were injected subcutaneously in the footpads of wt C57BL/6 mice preinjected with 40 ng of TNF-α s.c in the footpads 24 hours earlier. Recipient mice received CCP-treated DC (control) in the right footpad and CCP + GP1a–treated DCs in the left footpad. Forty-eight hours later, cells were collected from popliteal lymph nodes, and PKH-labeled cells were analyzed by FACS. Data from 3 different experiments are normalized by plotting the number of labeled cells from the control leg as 100%. (B) Supernatants collected from DC cultures before injection were analyzed for MMP-9 via ELISA.

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