| First Author | Song J | Year | 2016 |
| Journal | Eur J Immunol | Volume | 46 |
| Issue | 8 | Pages | 1878-86 |
| PubMed ID | 27218486 | Mgi Jnum | J:250207 |
| Mgi Id | MGI:5923100 | Doi | 10.1002/eji.201646396 |
| Citation | Song J, et al. (2016) The IgG1 B-cell receptor provides survival and proliferative signals analogue to the Igalpha but not the Igbeta co-receptor. Eur J Immunol 46(8):1878-86 |
| abstractText | The function of the IgM B-cell receptor (BCR) is dependent on intact signaling of the co-receptors Igalpha and Igbeta, both of which contain a cytoplasmic tail bearing an immunoreceptor tyrosine-based activation motif. We have previously demonstrated that the cytoplasmic tail of the IgG1 BCR can partially compensate for the loss of the signaling moiety of Igalpha. Here, we show that unlike Igalpha, Igbeta signaling is indispensable for the development and function of IgG1-expressing B cells. Deletion of the cytoplasmic signaling tail of Igbeta compromised the survival and proliferation not only of IgM(+) B cells but also of IgG1-expressing B cells. In the absence of the signaling tail of Igbeta, the transcription levels of the antiapoptotic gene bcl-xl and the cell-cycle gene ccnd2 were reduced, consistent with the observed defects in survival and proliferation. These results demonstrate functional differences between Igalpha and Igbeta in the transduction of IgG1 BCR signal. |
