hFCER1A(2)/hIGHE

Fig.1 Detection of human IgHE expression in serum by ELISA. 

Serum was collected from wild-type C57BL/6 mice (WT) and homozygous hFCER1A/hIGHE mice (HO/HO) (n=2, female, 6 weeks old). Protein expression level of human IGHE was analyzed by ELISA. 

The human IgE Elisa kit cross-reacted with mouse IgE and humanized IgE.

Fig.2 Detection of hFCER1A expression on CD117+ cells in peritoneal lavage fluid of WT C57BL/6 mice and hFCER1A/hIGHE mice by FACS. Leukocytes were collected from wild-type (WT) C57BL/6 mice (male, 9 weeks old) and homozygous(HO) hFCGR1A mice (male, 9-10 weeks old), and analyzed by flow cytometry with anti-mFCER1A and anti-hFCER1A. hFCER1A was exclusively detectable in hFCER1A/hIGHE humanized mice but not in wild-type mice. hFCER1A was exclusively detectable on CD117+ cells in hFCER1A/hIGHE humanized mice, whereas mFCER1A was exclusively detectable on CD117+ cells in wild-type C57BL/6 mice.

Fig.3 Effects of Omalizumab on OVA-induced ASA. hFCER1A(2)/hIGHE mice (HO/HO) were immunized with OVA/Al(OH)3 on day 0 and day 7, and challenged with OVA on day 14. Omalizumab was injected 3 hours before the challenge on day 14. The rectal temperature of the mice was recorded from 0 to 90 minutes after the challenge. The results showed that Omalizumab had an inhibitory effect on the decrease in rectal temperature caused by ASA modeling in hFCER1A(2)/hIGHE mice (HO/HO). 

Abbr. HO, homozygous;