1. Increased Phagocyte FcγRI Expression and Improved Fcγ-Receptor–Mediated Phagocytosis After In Vivo Recombinant Human Interferon-γ Treatment of Normal Human Subjects
by Deborah E. Schiff, Julie Rae, Thomas R. Martin, Bruce H. Davis, and John T. Curnutte
Blood
Volume 90(8):
October 15, 1997
©1997 by American Society of Hematology

2. Effect of rhIFN-γ on peripheral blood leukocyte counts.
Effect of rhIFN-γ on peripheral blood leukocyte counts. Mean ± SE leukocyte (•) and neutrophil (○) counts after in vivo rhIFN-γ (0.05 mg/m2 SC daily for 2 doses) administered to 16 healthy volunteers are shown. Asterisks indicate statistical significance (P < .05).
Deborah E. Schiff et al. Blood 1997;90:
©1997 by American Society of Hematology

3. Effect of in vivo rhIFN-γ administration on FcγRI expression on circulating neutrophils.
Effect of in vivo rhIFN-γ administration on FcγRI expression on circulating neutrophils. FcγRI expression was measured by flow cytometry as described in the Materials and Methods. Expression is depicted as FITC MESF ± SE for 12 healthy volunteers (•) and 6 untreated controls (○). Asterisks indicate statistical significance (P < .05)‏
Deborah E. Schiff et al. Blood 1997;90:
©1997 by American Society of Hematology

4. The effect of in vivo rhIFN-γ administration on monocyte surface molecule expression.
The effect of in vivo rhIFN-γ administration on monocyte surface molecule expression. In vivo rhIFN-γ was associated with a significant increase in expression of FcγRI (A), FcγRII (B), FcγRIII (C), HLA-DR (D), CD11a (F ), CD11b (G), and CD18 (H). Monocyte expression of CD14 (E) failed to change significantly. Results are reported as FITC MESF ± SE from patients (•; n = 12) who received rhIFN-γ per protocol and untreated normal controls (○; n = 6). Asterisks indicate statistical significance (P < .05).
Deborah E. Schiff et al. Blood 1997;90:
©1997 by American Society of Hematology

5. The effect of in vivo rhIFN-γ on bacterial ingestion by neutrophils.
The effect of in vivo rhIFN-γ on bacterial ingestion by neutrophils. These graphs show the mean ± SE phagocytosis by neutrophils of S aureus-BODIPY BioParticles opsonized with complement-depleted serum (A; •; n = 6) or pooled human serum with intact complement (B; ○; n = 4). Phagocytosis by neutrophils from rhIFN-γ–treated subjects was calculated as MFI (subject)/MFI (control) × 100. Asterisks indicate statistical significance (P < .05).
Deborah E. Schiff et al. Blood 1997;90:
©1997 by American Society of Hematology

6. Correlation of FcγRI expression by neutrophils with phagocytosis by neutrophils of S aureus opsonized with complement-depleted pooled human serum.
Correlation of FcγRI expression by neutrophils with phagocytosis by neutrophils of S aureus opsonized with complement-depleted pooled human serum. FcγRI expression by neutrophils from study subjects was determined by direct immunostaining before and after in vivo rhIFN-γ administration (0.05 mg/m2 SC daily for 2 days). Correlation of FcγRI expression by neutrophils with their ability to perform phagocytosis of HI-PHS–opsonized S aureus BioParticles was determined by regression analysis. FcγRI expression by neutrophils correlated directly with ability to ingest HI-PHS–opsonized S aureus (r = .8, P < .05).
Deborah E. Schiff et al. Blood 1997;90:
©1997 by American Society of Hematology

7. The effects of FcγRI antagonists on rhIFN-γ–enhanced bacterial ingestion by neutrophils.
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).
Deborah E. Schiff et al. Blood 1997;90:
©1997 by American Society of Hematology