Figure 6.
Figure 6. TNF-α activation of ECs, not leukocytes, appears to be responsible for the induction of leukocyte-EC interaction upon TNF-α treatment. WT cremaster muscle was transplanted to either p75−/− or WT mice. Following cremaster transplantation, the animal was kept for an equilibration period of 15 minutes. TNF-α (2 ng/mL, 25 μL) was applied directly to a 25-μm2 area of the cremaster muscle flap. Number of rolling and adherent leukocytes was counted in a time window of 2 minutes, in a 100-μm viewing segment. Control counts were obtained prior to TNF-α application. Values shown are the average number of rolling leukocytes or adhering leukocytes from 3 independent experiments. (○) WT cremaster to WT mice (rolling), (•) WT cremaster to p75−/− mice (rolling), (□) WT cremaster to WT mice (adhesion), (▪) WT cremaster to p75−/− mice (adhesion).

TNF-α activation of ECs, not leukocytes, appears to be responsible for the induction of leukocyte-EC interaction upon TNF-α treatment. WT cremaster muscle was transplanted to either p75−/− or WT mice. Following cremaster transplantation, the animal was kept for an equilibration period of 15 minutes. TNF-α (2 ng/mL, 25 μL) was applied directly to a 25-μm2 area of the cremaster muscle flap. Number of rolling and adherent leukocytes was counted in a time window of 2 minutes, in a 100-μm viewing segment. Control counts were obtained prior to TNF-α application. Values shown are the average number of rolling leukocytes or adhering leukocytes from 3 independent experiments. (○) WT cremaster to WT mice (rolling), (•) WT cremaster to p75−/− mice (rolling), (□) WT cremaster to WT mice (adhesion), (▪) WT cremaster to p75−/− mice (adhesion).

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