The Journal of Experimental Medicine
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Published online
doi:10.1084/jem.20081242
The Journal of Experimental Medicine, Vol. 206, No. 1, 51-59
The Rockefeller University Press, 0022-1007 $30.00
© Cruz-Guilloty et al.
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BRIEF DEFINITIVE REPORT

 Runx3 and T-box proteins cooperate to establish the transcriptional program of effector CTLs

Fernando Cruz-Guilloty1, Matthew E. Pipkin1, Ivana M. Djuretic1, Ditsa Levanon2, Joseph Lotem2, Mathias G. Lichtenheld3, Yoram Groner2, and Anjana Rao1

1 Harvard Medical School and the Immune Disease Institute, Boston, MA 02115
2 Department of Molecular Genetics, The Weizmann Institute of Science, Rehovot 76100, Israel
3 Department of Microbiology and Immunology, Sylvester Comprehensive Cancer Center, Miller School of Medicine, University of Miami, Miami, FL 10016

CORRESPONDENCE Anjana Rao: arao{at}idi.harvard.edu

Activation of naive CD8+ T cells with antigen induces their differentiation into effector cytolytic T lymphocytes (CTLs). CTLs lyse infected or aberrant target cells by exocytosis of lytic granules containing the pore-forming protein perforin and a family of proteases termed granzymes. We show that effector CTL differentiation occurs in two sequential phases in vitro, characterized by early induction of T-bet and late induction of Eomesodermin (Eomes), T-box transcription factors that regulate the early and late phases of interferon (IFN) {gamma} expression, respectively. In addition, we demonstrate a critical role for the transcription factor Runx3 in CTL differentiation. Runx3 regulates Eomes expression as well as expression of three cardinal markers of the effector CTL program: IFN-{gamma}, perforin, and granzyme B. Our data point to the existence of an elaborate transcriptional network in which Runx3 initially induces and then cooperates with T-box transcription factors to regulate gene transcription in differentiating CTLs.

F. Cruz-Guilloty and M.E. Pipkin contributed equally to this paper.

© 2009 Cruz-Guilloty et al.
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