Fig. 5.
Fig. 5. Effect of α-CXCR–1 and α-CXCR–2 antibodies on NAP-2–induced neutrophil chemotaxis. Neutrophils were left untreated (○) or preincubated (•) with α-CXCR–2 antibody RII115 (A), α-CXCR– antibody SE-2 (B) or a combination of both antibodies (C) for 60 minutes. The concentration of each antibody was 100 μg/mL. As a control, PMN were incubated with both antibodies in the presence of the peptides CXCR-1[1-30] and CXCR-2[6-29] (D). Subsequently, the cells were assayed for chemotaxis in response to increasing concentrations of NAP-2. Data represent mean ± SD of four different experiments (A and B) or mean ± deviation from single values of two independent experiments (C and D). Random migration of untreated cells (- - -) did not significantly differ from migration of cells incubated with the antibodies in the absence of the chemokines.

Effect of α-CXCR–1 and α-CXCR–2 antibodies on NAP-2–induced neutrophil chemotaxis. Neutrophils were left untreated (○) or preincubated (•) with α-CXCR–2 antibody RII115 (A), α-CXCR– antibody SE-2 (B) or a combination of both antibodies (C) for 60 minutes. The concentration of each antibody was 100 μg/mL. As a control, PMN were incubated with both antibodies in the presence of the peptides CXCR-1[1-30] and CXCR-2[6-29] (D). Subsequently, the cells were assayed for chemotaxis in response to increasing concentrations of NAP-2. Data represent mean ± SD of four different experiments (A and B) or mean ± deviation from single values of two independent experiments (C and D). Random migration of untreated cells (- - -) did not significantly differ from migration of cells incubated with the antibodies in the absence of the chemokines.

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