| First Author | Anzelon AN | Year | 2003 |
| Journal | Nat Immunol | Volume | 4 |
| Issue | 3 | Pages | 287-94 |
| PubMed ID | 12563260 | Mgi Jnum | J:83213 |
| Mgi Id | MGI:2658752 | Doi | 10.1038/ni892 |
| Citation | Anzelon AN, et al. (2003) Pten inactivation alters peripheral B lymphocyte fate and reconstitutes CD19 function. Nat Immunol 4(3):287-94 |
| abstractText | Phosphoinositide 3-kinase (PI3K) and phosphatase and tensin homolog (PTEN) phosphatase serve essential functions in the regulation of cell growth, differentiation and survival by modulating intracellular phosphatidylinositol-3,4,5-trisphosphate (PI-3,4,5-P3) concentrations. Here we show that the conditional deletion of Pten in B cells led to the preferential generation of marginal zone (MZ) B cells and B1 cells. PTEN-deficient B cells were hyperproliferative in response to mitogenic stimuli, and exhibited a lower threshold for activation through the B cell antigen receptor. Inactivation of PTEN rescued germinal center, MZ B and B1 cell formation in CD19-/- mice, arguing that recruitment and activation of PI3K are the dominant roles for CD19 in these B cell subpopulations. These findings establish the central role of PI-3,4,5-P3 regulation in the differentiation of peripheral B cell subsets. |
