Fig. 5.
Fig. 5. IL-4–induced adhesion of cultured human mast cells to immobilized ICAM-1. After the cells were preincubated with (▪) or without (□) IL-4 (10 ng/mL) for 3 days, cultured human mast cells were incubated in ICAM-1 (2 μg/well)-, or BSA (1%)-coated wells. Indicated blocking antibodies (20 μg/mL) were added to each well. Cell binding (%) was measured and calculated as described in Materials and Methods. Each value represents mean ±SD (bar) of triplicate samples. IL-4–treated mast cells showed statistically significant binding ability to ICAM-1 compared with IL-4–nontreated mast cells (P < .001). This IL-4–induced binding to ICAM-1 was inhibited by TS1/22 (anti–LFA-1α MoAb) (P < .005), TS1/18 (anti–LFA-1β MoAb) (P < .001), and RR1/1 (anti–ICAM-1 MoAb) (P < .001). Similar results were obtained in three independent experiments.

IL-4–induced adhesion of cultured human mast cells to immobilized ICAM-1. After the cells were preincubated with (▪) or without (□) IL-4 (10 ng/mL) for 3 days, cultured human mast cells were incubated in ICAM-1 (2 μg/well)-, or BSA (1%)-coated wells. Indicated blocking antibodies (20 μg/mL) were added to each well. Cell binding (%) was measured and calculated as described in Materials and Methods. Each value represents mean ±SD (bar) of triplicate samples. IL-4–treated mast cells showed statistically significant binding ability to ICAM-1 compared with IL-4–nontreated mast cells (P < .001). This IL-4–induced binding to ICAM-1 was inhibited by TS1/22 (anti–LFA-1α MoAb) (P < .005), TS1/18 (anti–LFA-1β MoAb) (P < .001), and RR1/1 (anti–ICAM-1 MoAb) (P < .001). Similar results were obtained in three independent experiments.

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