| First Author | Fujiwara H | Year | 1994 |
| Journal | Proc Natl Acad Sci U S A | Volume | 91 |
| Issue | 15 | Pages | 6835-9 |
| PubMed ID | 8041705 | Mgi Jnum | J:19437 |
| Mgi Id | MGI:67606 | Doi | 10.1073/pnas.91.15.6835 |
| Citation | Fujiwara H, et al. (1994) The absence of IgE antibody-mediated augmentation of immune responses in CD23-deficient mice. Proc Natl Acad Sci U S A 91(15):6835-9 |
| abstractText | The CD23 antigen, a low-affinity receptor for IgE (Fc epsilon RII), is a type II membrane-bound glycoprotein expressed on various cells, particularly mature B cells. A number of functions have been ascribed to CD23, including specific regulation of IgE production, IgE-mediated cytotoxicity and release of mediators, IgE-dependent antigen focusing, promotion of B-cell growth, prevention of germinal center B cells from apoptosis, proliferation of myeloid precursors, and maturation of early thymocytes. It is not clear whether these activities represent in vivo functions. To explore in vivo functions of CD23, we have produced CD23-deficient mice. These mice displayed normal lymphocyte differentiation and could mount normal antibody responses, including IgE responses upon immunization with T-dependent antigens and infection with Nippostrongyrus brasiliensis. Germinal center formation after immunization and in vitro proliferative response of B cells were not affected in mutant mice. However, antigen-specific IgE-mediated enhancement of antibody responses was severely impaired. |
