| First Author | Crowley JE | Year | 2009 |
| Journal | Blood | Volume | 113 |
| Issue | 7 | Pages | 1464-73 |
| PubMed ID | 18791164 | Mgi Jnum | J:145457 |
| Mgi Id | MGI:3834778 | Doi | 10.1182/blood-2008-02-138651 |
| Citation | Crowley JE, et al. (2009) FcgammaRIIB signals inhibit BLyS signaling and BCR-mediated BLyS receptor up-regulation. Blood 113(7):1464-73 |
| abstractText | These studies investigate how interactions between the BCR and FcgammaRIIB affect B lymphocyte stimulator (BLyS) recep-tor expression and signaling. Previous studies showed that BCR ligation up-regulates BLyS binding capacity in mature B cells, reflecting increased BLyS receptor levels. Here we show that FcgammaRIIB coaggregation dampens BCR-induced BLyS receptor up-regulation. This cross-regulation requires BCR and FcgammaRIIB coligation, and optimal action relies on the Src-homology-2 (SH2)-containing inositol 5 phosphase-1 (SHIP1). Subsequent to FcgammaRIIB/BCR coaggregation, the survival promoting actions of BLyS are attenuated, reflecting reduced BLyS receptor signaling capacity in terms of Pim 2 maintenance, noncanonical NF-kappaB activation, and Bcl-xL levels. These findings link the negative regulatory functions of FcgammaRIIB with BLyS-mediated B-cell survival. |
