| First Author | Halcomb KE | Year | 2007 |
| Journal | Eur J Immunol | Volume | 37 |
| Issue | 4 | Pages | 1033-42 |
| PubMed ID | 17372989 | Mgi Jnum | J:120843 |
| Mgi Id | MGI:3708070 | Doi | 10.1002/eji.200636451 |
| Citation | Halcomb KE, et al. (2007) Btk and phospholipase Cgamma2 can function independently during B cell development. Eur J Immunol 37(4):1033-42 |
| abstractText | The pre-BCR and the BCR regulate B cell development via a signalosome nucleated by the adaptor protein B cell linker protein (BLNK). Formation of this complex facilitates activation of phospholipase C (PLC) gamma2 by Bruton's tyrosine kinase (Btk). To determine whether Btk and PLCgamma2 also have separate functions, we generated Btk(-/-)PLCgamma2(-/-) mice. They demonstrated a block in development at the pre-B stage and increased pre-BCR surface expression. This phenotype was more severe than that of Btk(-/-) or PLCgamma2(-/-) mice. Although both Btk and PLCgamma2 were required for proliferation of splenic B cells in response to BCR cross-linking, they contributed differently to anti-IgM-induced phosphorylation of ERK. Btk(-/-) and PLCgamma2(-/-) mice each had a reduced frequency of Iglambda-expressing B cells and impaired migration of pre-B cells towards stromal cell-derived factor 1. However, the increase in pre-B cell malignancy that occurs in BLNK(-/-) mice in the absence of Btk was not observed in the absence of PLCgamma2. Thus, Btk and PLCgamma2 act both in concert and independently throughout B cell development. |
