| First Author | Lutz C | Year | 1998 |
| Journal | Nature | Volume | 393 |
| Issue | 6687 | Pages | 797-801 |
| PubMed ID | 9655395 | Mgi Jnum | J:57600 |
| Mgi Id | MGI:1344994 | Doi | 10.1038/31716 |
| Citation | Lutz C, et al. (1998) IgD can largely substitute for loss of IgM function in B cells. Nature 393(6687):797-801 |
| abstractText | The mu and delta heavy chains of IgM and IgD, the first antibody isotypes expressed during bone-marrow B-cell development, are encoded by a common transcription unit. Expression of the mu chain on the surface of late pre-B cells allows their further development to immature B cells. Coexpression of the delta chain and emigration of the immature B cells to the periphery eventually leads to the development of naive mature IgM/IgD double-positive cells. Although IgM is important in driving B-cell development, the contribution of IgD is not clear. Here we investigate the function of IgD. We generated mice deficient in IgM (IgM-/- mice) by deleting the mu region in embryonic stem cells. IgM-/- mice showed normal B-cell development and maturation, with IgD replacing membrane-bound and secretory IgM. Moreover, specific B-cell responses and isotype class switches occurred during immunization or infection. In contrast to mice deficient in B cells, IgM-/- mice survived infection with vesicular stomatitis virus by developing neutralizing immunoglobulins, but they were more susceptible than wild-type controls with delayed specific immunoglobulin responses. These data lead us to conclude that IgD is largely able to substitute for IgM functions. |
