The Journal of Experimental Medicine
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Published online August 13, 2007
doi:10.1084/jem.20070841
The Journal of Experimental Medicine, Vol. 204, No. 9, 2015-2021
The Rockefeller University Press, 0022-1007 $30.00
© 2007 Intlekofer et al.
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BRIEF DEFINITIVE REPORT

 Requirement for T-bet in the aberrant differentiation of unhelped memory CD8+ T cells

Andrew M. Intlekofer1,2, Naofumi Takemoto1,2, Charlly Kao4, Arnob Banerjee1,2, Felix Schambach1,2, John K. Northrop3, Hao Shen3, E. John Wherry4, and Steven L. Reiner1,2

1 Abramson Family Cancer Research Institute, 2 Department of Medicine, and 3 Department of Microbiology, University of Pennsylvania, Philadelphia, PA 19104
4 Immunology Program, The Wistar Institute, Philadelphia, PA 19104

CORRESPONDENCE Steven L. Reiner: sreiner{at}mail.med.upenn.edu

Immunity to intracellular pathogens requires dynamic balance between terminal differentiation of short-lived, cytotoxic effector CD8+ T cells and self-renewal of central–memory CD8+ T cells. We now show that T-bet represses transcription of IL-7R{alpha} and drives differentiation of effector and effector–memory CD8+ T cells at the expense of central–memory cells. We also found T-bet to be overexpressed in CD8+ T cells that differentiated in the absence of CD4+ T cell help, a condition that is associated with defective central–memory formation. Finally, deletion of T-bet corrected the abnormal phenotypic and functional properties of "unhelped" memory CD8+ T cells. T-bet, thus, appears to function as a molecular switch between central– and effector–memory cell differentiation. Antagonism of T-bet may, therefore, represent a novel strategy to offset dysfunctional programming of memory CD8+ T cells.

Abbreviation used: LCMV, lymphocytic choriomeningitis virus.


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