| First Author | Chan VW | Year | 1997 |
| Journal | Immunity | Volume | 7 |
| Issue | 1 | Pages | 69-81 |
| PubMed ID | 9252121 | Mgi Jnum | J:42037 |
| Mgi Id | MGI:894972 | Doi | 10.1016/s1074-7613(00)80511-7 |
| Citation | Chan VW, et al. (1997) Characterization of the B lymphocyte populations in Lyn-deficient mice and the role of Lyn in signal initiation and down-regulation. Immunity 7(1):69-81 |
| abstractText | Lyn-deficient mice were generated to analyze the role of Lyn in B cell antigen receptor (BCR) signaling. These mice had a reduced number of peripheral B cells with a greater proportion of immature cells and a higher than normal turnover rate. Aged lyn-/- mice developed splenomegaly, produced autoantibodies, and had an expanded population of B lymphoblasts of the B1 lineage. Splenic B cells from young lyn-/- mice initiated early BCR signaling events, although in a delayed fashion. Unexpectedly, lyn-/- B cells exhibited an enhanced MAP kinase activation and an increased proliferative response to BCR engagement. Stimulation of lyn-/- B cells with intact and F(ab')2 anti-IgM revealed defects in at least two mechanisms that negatively regulate BCR signaling, one of which involves Fc gammaRIIb1. |
