Fig. 6.
Fig. 6. The effects of FcγRI antagonists on rhIFN-γ–enhanced bacterial ingestion by neutrophils. The graph shows the effect of anti-FcγRI MoAb (197) and F(ab′)2 (32.2), and control murine IgG2a (mIgG2a) and murine F(ab′)2 [mF(ab′)2 ] on phagocytosis of HI-PHS–opsonized S aureus-BODIPY BioParticles by neutrophils. The mean MFI of neutrophils obtained from two different study subjects (□) before in vivo rhIFN-γ administration (0.05 mg/m2/dose SC daily for 2 days) and (▪) 48 hours after the initiation of in vivo rhIFN-γ treatment are depicted. Asterisks indicate statistically significant inhibition by the MoAb or F(ab′)2 when compared with the corresponding 48-hour control in which no MoAb or F(ab′)2 was present (Student's t-test, P < .05).

The effects of FcγRI antagonists on rhIFN-γ–enhanced bacterial ingestion by neutrophils. The graph shows the effect of anti-FcγRI MoAb (197) and F(ab′)2 (32.2), and control murine IgG2a (mIgG2a) and murine F(ab′)2 [mF(ab′)2 ] on phagocytosis of HI-PHS–opsonized S aureus-BODIPY BioParticles by neutrophils. The mean MFI of neutrophils obtained from two different study subjects (□) before in vivo rhIFN-γ administration (0.05 mg/m2/dose SC daily for 2 days) and (▪) 48 hours after the initiation of in vivo rhIFN-γ treatment are depicted. Asterisks indicate statistically significant inhibition by the MoAb or F(ab′)2 when compared with the corresponding 48-hour control in which no MoAb or F(ab′)2 was present (Student's t-test, P < .05).

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