First Author | Harada M | Year | 1989 |
Journal | Immunol Invest | Volume | 18 |
Issue | 5 | Pages | 723-35 |
PubMed ID | 2737701 | Mgi Jnum | J:9853 |
Mgi Id | MGI:58310 | Doi | 10.3109/08820138909057758 |
Citation | Harada M, et al. (1989) Strain difference and mode of inheritance of the susceptibility to passive cutaneous anaphylaxis mediated by allogeneic IgE antibody in the mouse. Immunol Invest 18(5):723-35 |
abstractText | The strain difference and mode of inheritance of the susceptibility to PCA (passive cutaneous anaphylaxis) were studied in mice. No marked strain differences were found in the susceptibility to PCA mediated by allogeneic IgG1 monoclonal and xenogeneic IgG antibodies, although BALB/c Crj mice were somewhat less susceptible than the other strains. On the other hand, the susceptibility to PCA mediated by allogeneic IgE monoclonal antibodies differed greatly according to the strain; SJL/J, A.SW/J and DS/Shi mice being highly susceptible and C57BL/6JShi, BALB/cCrj, DBA/2Crj, C3H/HeShi and CBA/JNCrj mice insusceptible. Based on the marked difference between DS/Shi and C3H/HeShi strains, the mode of inheritance of the susceptibility to IgE PCA was studied using their F1, F2 and F1 x parent backcross offspring. All the F1 hybrids by reciprocal crosses between these two strains and F1 x DS backcross mice were highly susceptible like DS/Shi mice. Backcross mice between F1 and C3H/HeShi showed approximately 1:1 segregation into the susceptible and insusceptible. Segregation was also observed in the F2 generation; 32% being insusceptible. These results suggest that the high susceptibility is a dominant phenotype controlled mainly by a single gene on an autosomal chromosome; this was statistically supported by tests of the segregation ratios obtained. However, in the PCA-positive recipients of F1 x C3H backcross and F2 generations, dye leakage into the skin was tended to be diffuse and less compact than in DS/Shi, F1 and F1 x DS backcross mice. This suggests the presence of some additional genes which modify the expression of the main gene. |