Strain specific IgE expression analysis in homozygous B-hIgE/hFCER1A mice by flow cytometry. Basophilic granulocytes of the bone marrow were collected from wild-type C57BL/6 mice (+/+) and homozygous B-hIgE/hFCER1A mice (H/H;H/H) stimulated with LPS in vivo, and analyzed by flow cytometry with species-specific anti-IgE antibody. Mouse IgE was detectable in WT mice (+/+). Human IgE was exclusively detectable in homozygous B-hIgE/hFCER1A mice (H/H;H/H) but not in WT mice (+/+).

Strain specific FCER1A expression analysis in homozygous B-hIgE/hFCER1A mice by flow cytometry. Basophilic granulocytes of the bone marrow were collected from wild type (WT) mice (+/+) and homozygous B-hIgE/hFCER1A mice (H/H;H/H), and analyzed by flow cytometry with species-specific anti-FCER1A antibody. Mouse FCER1A was detectable in WT mice (+/+). Human FCER1A was exclusively detectable in homozygous B-hIgE/hFCER1A mice (H/H;H/H) but not in WT mice (+/+).

Effects of Omalizumab on OVA induced ASA. B-hIgE/hFCER1A mice (H/H; H/H) received OVA/Al(OH)3 immunization on day 0, and challenge with OVA on day 14. Omalizumab (in house) was injected 3 hour before challenge on day 14. (A) The body temperature of the mice was recorded from 0 to 90 minutes after the challenge. (B) An increasing trend was produced by Omalizumab (in house) in the ASA model. It can be seen that Omalizumab (in house) has an inhibitory effect on the decrease in body temperature caused by ASA modeling in B-hIgE/hFCER1A mice (H/H; H/H).