| First Author | Ford JW | Year | 2009 |
| Journal | Cell Immunol | Volume | 254 |
| Issue | 2 | Pages | 124-34 |
| PubMed ID | 18828998 | Mgi Jnum | J:142807 |
| Mgi Id | MGI:3822218 | Doi | 10.1016/j.cellimm.2008.08.003 |
| Citation | Ford JW, et al. (2009) 129/SvJ mice have mutated CD23 and hyper IgE. Cell Immunol 254(2):124-34 |
| abstractText | CD23, the low affinity IgE receptor, is hypothesized to function as a negative regulator of IgE production. Upon discovering reduced CD23 surface levels in 129/SvJ inbred mice, we sought to further investigate 129/SvJ CD23 and to examine its influence on IgE levels. Five amino acid substitutions were found in 129/SvJ CD23. Identical mutations were also observed in CD23 from New Zealand Black and 129P1/ReJ mice. 129/SvJ B cells proliferated more rapidly than those from BALB/c after stimulation with IL-4 and CD40 ligand trimer. However, in vitro IgE levels in supernatants from stimulated 129/SvJ B cells were significantly reduced. Contrary to the in vitro findings, the 129/SvJ CD23 mutations correlated with a hyper IgE phenotype in vivo and 129/SvJ were able to clear Nippostrongylus brasiliensis infection more rapidly than either BALB/c or C57BL/6. Overall, this study further suggests that CD23 is an important regulatory factor for IgE production. |
