| First Author | Jumaa H | Year | 1999 |
| Journal | Immunity | Volume | 11 |
| Issue | 5 | Pages | 547-54 |
| PubMed ID | 10591180 | Mgi Jnum | J:58740 |
| Mgi Id | MGI:1349543 | Doi | 10.1016/s1074-7613(00)80130-2 |
| Citation | Jumaa H, et al. (1999) Abnormal development and function of B lymphocytes in mice deficient for the signaling adaptor protein SLP-65. Immunity 11(5):547-54 |
| abstractText | During signal transduction through the B cell antigen receptor (BCR), several signaling elements are brought together by the adaptor protein SLP-65. We have investigated the role of SLP-65 in B cell maturation and function in mice deficient for SLP-65. While the mice are viable, B cell development is affected at several stages. SLP-65-deficient mice show increased proportions of pre-B cells in the bone marrow and immature B cells in peripheral lymphoid organs. B1 B cells are lacking. The mice show lower IgM and IgG3 serum titers and poor IgM but normal IgG immune responses. Mutant B cells show reduced Ca2+ mobilization and reduced proliferative responses to B cell mitogens. We conclude that while playing an important role, SLP-65 is not always required for signaling from the BCR. |
