| First Author | Nopora A | Year | 2002 |
| Journal | J Immunol | Volume | 169 |
| Issue | 6 | Pages | 3006-14 |
| PubMed ID | 12218115 | Mgi Jnum | J:132008 |
| Mgi Id | MGI:3774927 | Doi | 10.4049/jimmunol.169.6.3006 |
| Citation | Nopora A, et al. (2002) Bcl-2 controls dendritic cell longevity in vivo. J Immunol 169(6):3006-14 |
| abstractText | Dendritic cells (DC) were found to down-regulate Bcl-2 protein upon maturation in vivo. Because Bcl-2 has been shown to exert anti-apoptotic functions, down-regulation of Bcl-2 could be a mechanism by which DC longevity is controlled. To dysregulate this potential control system and to study the role of Bcl-2 in DC, we expressed human Bcl-2 under control of the murine CD11c-promoter as a transgene specifically in DC and show that DC frequencies and numbers increase in transgenic mice. In vivo bromodeoxyuridin, as well as adoptive, DC transfer studies show that the relative turnover/survival of mature Bcl-2 transgenic DC is increased. This had a direct impact on CD4+ T cell, as well as humoral immune, responses, which were elevated in transgenic animals. When Bcl-2 transgenic DC were used as DC vaccines, they induced 2- to 3-fold greater expansion of Ag-specific CTL, and stronger in vivo cytotoxicity. Overall, these data indicate that down-regulation of Bcl-2 controls DC longevity, which in turn directly regulates immune responses and the efficacy of DC when used as vaccines. |
