| Title | B cell development is arrested at the immature B cell stage in mice carrying a mutation in the cytoplasmic domain of immunoglobulin beta. |
| Publication Type | Journal Article |
| Year of Publication | 2001 |
| Authors | Reichlin A, Hu Y, Meffre E, Nagaoka H, Gong S, Kraus M, Rajewsky K, Nussenzweig MC |
| Journal | J Exp Med |
| Volume | 193 |
| Issue | 1 |
| Pagination | 13-23 |
| Date Published | 2001 Jan 01 |
| ISSN | 0022-1007 |
| Keywords | Alleles, Animals, Apoptosis, B-Lymphocytes, Base Sequence, Calcium Signaling, Cell Differentiation, DNA Primers, Immunoglobulin D, Immunoglobulin M, Mice, Mice, Knockout, Mice, Transgenic, Mutation, Receptors, Antigen, B-Cell, Signal Transduction |
| Abstract | The B cell receptor (BCR) regulates B cell development and function through immunoglobulin (Ig)alpha and Ig beta, a pair of membrane-bound Ig superfamily proteins, each of which contains a single cytoplasmic immunoreceptor tyrosine activation motif (ITAM). To determine the function of Ig beta, we produced mice that carry a deletion of the cytoplasmic domain of Ig beta (Ig beta Delta C mice) and compared them to mice that carry a similar mutation in Ig alpha (MB1 Delta C, herein referred to as Ig alpha Delta C mice). Ig beta Delta C mice differ from Ig alpha Delta C mice in that they show little impairment in early B cell development and they produce immature B cells that respond normally to BCR cross-linking as determined by Ca(2+) flux. However, Ig beta Delta C B cells are arrested at the immature stage of B cell development in the bone marrow and die by apoptosis. We conclude that the cytoplasmic domain Ig beta is required for B cell development beyond the immature B cell stage and that Ig alpha and Ig beta have distinct biologic activities in vivo. |
| Alternate Journal | J. Exp. Med. |
| PubMed ID | 11136817 |
| PubMed Central ID | PMC2195879 |
| Grant List | KO8 / / PHS HHS / United States |