| First Author | Powzaniuk MA | Year | 2001 |
| Journal | J Immunol | Volume | 167 |
| Issue | 1 | Pages | 242-9 |
| PubMed ID | 11418655 | Mgi Jnum | J:132591 |
| Mgi Id | MGI:3776337 | Doi | 10.4049/jimmunol.167.1.242 |
| Citation | Powzaniuk MA, et al. (2001) B-Myb overexpression results in activation and increased Fas/Fas ligand-mediated cytotoxicity of T and NK cells. J Immunol 167(1):242-9 |
| abstractText | The human B-myb gene encodes a transcriptional regulator that plays an important role in cell cycle progression, differentiation, and survival. To assess the in vivo role of B-myb, we investigated the phenotype of mouse transgenic lines in which B-Myb expression in lymphoid tissues was driven by the LCK proximal promoter. Overexpression of B-Myb had no measurable effect on the subsets of splenic and thymic lymphocytes, but was associated with increased expression of Fas ligand in NK and T cells. B-Myb-overexpressing splenocytes expressed higher IFN-gamma levels and contained higher percentages of cytokine-producing cells than wild-type (wt) splenocytes, as detected by Western blot analysis and ELISPOT assays, respectively. Ex vivo-cultured transgenic thymocytes and splenocytes had decreased survival compared with the corresponding cells from wt mice, possibly dependent on increased expression of Fas ligand. In addition, Fas ligand-dependent cytotoxicity of transgenic T and NK cells was significantly higher than that mediated by their wt counterparts. Together, these results indicate that B-Myb overexpression results in T and NK cell activation and increased cytotoxicity. Therefore, in addition to its well-established role in proliferation and differentiation, B-myb also appears to be involved in activation of NK and T cells and in their regulation of Fas/Fas ligand-mediated cytotoxicity |
