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 Blood, 1 April 2006, Vol. 107, No. 7, pp. 2797-2805.
Prepublished online as a Blood First Edition Paper on December 15, 2005; DOI 10.1182/blood-2005-08-3103.

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IMMUNOBIOLOGY

T-bet concomitantly controls migration, survival, and effector functions during the development of V{alpha}14i NKT cells

Jennifer L. Matsuda, Qianjun Zhang, Rachel Ndonye, Stewart K. Richardson, Amy R. Howell, and Laurent Gapin

From the Integrated Department of Immunology, National Jewish Medical and Research Center, University of Colorado Health Science Center, Denver; and Department of Chemistry, University of Connecticut, Storrs.

V{alpha}14i natural killer T (NKT)–cell function has been implicated in a number of disease conditions. The molecular events that drive V{alpha}14i 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 V{alpha}14i NKT-cell lineage development. Microarray gene-expression analyses on developing V{alpha}14i NKT cells were performed and provide a molecular framework to study these maturation events. In vitro ectopic expression of T-bet in immature V{alpha}14i NKT cells, which do not yet express T-bet, was sufficient to promote V{alpha}14i 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 V{alpha}14i NKT cells and acts to link these attributes to a developmental process.


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