| First Author | Benatar T | Year | 1996 |
| Journal | J Exp Med | Volume | 183 |
| Issue | 1 | Pages | 329-34 |
| PubMed ID | 8551241 | Mgi Jnum | J:78888 |
| Mgi Id | MGI:2386431 | Doi | 10.1084/jem.183.1.329 |
| Citation | Benatar T, et al. (1996) Immunoglobulin-mediated signal transduction in B cells from CD45-deficient mice. J Exp Med 183(1):329-34 |
| abstractText | CD45 expression is essential for immunoglobulin (Ig)-mediated B cell activation. Treatments with either anti-Ig or anti-CD45 suggest that CD45 may facilitate early signaling events such as calcium mobilization, and phosphoinositide hydrolyis as well as later events leading to transcription of genes such as c-myc. To examine the role of CD45 more extensively, CD45-deficient mice were generated by disruption of exon 6. Although normal numbers of B cells were found in peripheral lymphoid tissues, CD45-deficient cells failed to proliferate upon IgM crosslinking. In the present study, we demonstrate that the fraction of high buoyant density B cells is reduced while low buoyant density cells are increased. Moreover, there is a significant decline in the number of splenic B cells of the mature IgDhi, IgMlo phenotype. Although both the basal and anti-Ig-induced levels of phosphorylation of Ig-alpha and phospholipase C gamma 2 are indistinguishable from that observed in CD45+ control B cells, a major distinction was found in Ca2+ mobilization. While anti-Ig-induced mobilization of intracellular Ca2+ stores was normal, influx from extracellular sources was abrogated. This finding reveals a novel pathway of regulating B cell responses mediated by CD45. |
