| First Author | Matsuda JL | Year | 2006 |
| Journal | Blood | Volume | 107 |
| Issue | 7 | Pages | 2797-805 |
| PubMed ID | 16357323 | Mgi Jnum | J:131248 |
| Mgi Id | MGI:3773395 | Doi | 10.1182/blood-2005-08-3103 |
| Citation | Matsuda JL, et al. (2006) T-bet concomitantly controls migration, survival, and effector functions during the development of Valpha14i NKT cells. Blood 107(7):2797-805 |
| abstractText | Valpha14i natural killer T (NKT)-cell function has been implicated in a number of disease conditions. The molecular events that drive Valpha14i NKT-cell development remain elusive. We recently showed that T-bet is required for the terminal maturation of these cells. Here we identify some of the genetic targets of T-bet during Valpha14i NKT-cell lineage development. Microarray gene-expression analyses on developing Valpha14i NKT cells were performed and provide a molecular framework to study these maturation events. In vitro ectopic expression of T-bet in immature Valpha14i NKT cells, which do not yet express T-bet, was sufficient to promote Valpha14i NKT-cell maturation, driving the expression of multiple genes, including those that participate in migration, survival, and effector functions. By regulating the expression of T-helper 1 (Th1)-associated cytokines, chemokines, chemokine receptors, and molecules involved in cytolysis, T-bet defines the unique lineage attributes of mature Valpha14i NKT cells and acts to link these attributes to a developmental process. |
