| First Author | Dal Porto JM | Year | 2004 |
| Journal | Immunity | Volume | 21 |
| Issue | 3 | Pages | 443-53 |
| PubMed ID | 15357954 | Mgi Jnum | J:93928 |
| Mgi Id | MGI:3510277 | Doi | 10.1016/j.immuni.2004.07.018 |
| Citation | Dal Porto JM, et al. (2004) Regulation of BCR signal transduction in B-1 cells requires the expression of the Src family kinase Lck. Immunity 21(3):443-53 |
| abstractText | Although found predominantly in the peritoneal and pleural cavities, B-1 cells are also present in other peripheral tissues such as spleen and lung. While similar in surface phenotypes, such as CD5, all B-1 cells are not equivalent in their response to stimuli. Here, we report that the src family kinase Lck is required to confer the BCR hyporesponsiveness typical of CD5+ B-1 cells and appears involved in the maintenance of their unique function. Splenic B-1 cells express CD5 but not Lck and are not hyporesponsive; however, within the peritoneum, these B-1 cells are induced to express Lck and acquire a hyporesponsive phenotype. Peritoneal B-1 cells from lck-deficient mice, while CD5+, no longer exhibit attenuated BCR signaling. Interestingly, lck-null mice exhibited increased natural antibody levels characteristic of B-1 cells. Taken together, these results demonstrate a key role for Lck in modulating the signaling and cellular fate of B-1 B cells. |
