| First Author | Xu J | Year | 1994 |
| Journal | Immunity | Volume | 1 |
| Issue | 5 | Pages | 423-31 |
| PubMed ID | 7882172 | Mgi Jnum | J:25010 |
| Mgi Id | MGI:72725 | Doi | 10.1016/1074-7613(94)90073-6 |
| Citation | Xu J, et al. (1994) Mice deficient for the CD40 ligand [published erratum appears in Immunity 1994 Oct;1(7):following 613]. Immunity 1(5):423-31 |
| abstractText | To study the potential roles of CD40L in immune responses, we generated CD40L-deficient mice by gene targeting. Similar to the effects of CD40L mutations in humans (hyper-IgM syndrome), CD40L-deficient mice have a decreased IgM response to thymus-dependent antigens, fail altogether to produce an antigen-specific IgG1 response following immunization, yet respond normally to a T-independent antigen, TNP-Ficoll. Moreover, these mice do not develop germinal centers in response to thymus-dependent antigens, suggesting an inability to develop memory B cell responses. Although CD40L-deficient mice have low levels of most circulating immunoglobulin isotypes, they do not exhibit the spontaneous hyper-IgM syndrome seen in humans, at least up to 12 weeks of age. In summary, our study confirms the important role of CD40-CD40L interactions in thymus-dependent humoral immune responses and germinal center formation. |
