| First Author | Engel P | Year | 1995 |
| Journal | Immunity | Volume | 3 |
| Issue | 1 | Pages | 39-50 |
| PubMed ID | 7542548 | Mgi Jnum | J:27236 |
| Mgi Id | MGI:74653 | Doi | 10.1016/1074-7613(95)90157-4 |
| Citation | Engel P, et al. (1995) Abnormal B lymphocyte development, activation, and differentiation in mice that lack or overexpress the CD19 signal transduction molecule. Immunity 3(1):39-50 |
| abstractText | CD19-deficient mice were generated to examine the role of CD19 in B cell growth regulation in vivo. Deletion of CD19 had no deleterious effects on the generation of B cells in the bone marrow, but there was a significant reduction in the number of B cells in peripheral lymphoid tissues. B cells from CD19-deficient mice exhibited markedly decreased proliferative responses to mitogens, and serum immunoglobulin levels were also significantly decreased. In contrast, mice that overexpressed CD19 had significant defects in early B cell development in the bone marrow, augmented mitogenic responses, and increased serum immunoglobulin levels. These experiments indicate that CD19 functions to define signaling thresholds for cell surface receptors that regulate B lymphocyte selection, activation, and differentiation. |
