IgG-blocking antibodies inhibit IgE-mediated anaphylaxis in vivo through both antigen interception and FcγRIIb cross-linking
J. Clin. Invest. Richard T. Strait, et al. 116:833 doi:10.1172/JCI25575 [Go to this article.]

Figure 5
IgG BA inhibits IgE-mediated anaphylaxis through both FcγRIIb-dependent and -independent mechanisms. (A) WT and FcγRIIb-deficient mice (8–10 per group) were primed i.v. with 10 μg of IgEαTNP and treated i.v. with the quantities of αTNP Asm indicated on the graph abscissas. Mice were injected i.v. 24 hours later with 10 μg of biotin–anti–IL-4 mAb and challenged i.v. with 100 ng of TNP-OVA. Maximum temperature decreases during the 90 minutes after challenge were determined. Blood was drawn 2 hours after challenge, and IL-4 secretion was determined by IVCCA. All mice survived. (B) FcγRIII-deficient mice (5 per group) were primed i.v. with 10 μg of IgEαTNP and treated i.v. with the quantities of αTNP Asm indicated on the graph abscissas and s.c. with 500 μg of either anti–FcγRII/RIII mAb or isotype-matched control mAb. Mice were injected i.v. 24 hours later with 10 μg of biotin–anti–IL-4 mAb and challenged i.v. with 1 μg or 100 ng of TNP-OVA. Maximum temperature decreases during the 90 minutes after challenge were determined. Survival was 100% for all mice challenged with 100 ng of TNP-OVA and as indicated for mice challenged with 1 μg of TNP-OVA. Blood was drawn 2 hours after challenge, and IL-4 secretions were determined by IVCCA for mice challenged with 100 ng TNP-OVA. *P < 0.05. ^†P < 0.05 compared with control mAb–treated mice that received no αTNP Asm.