Control of Effector CD8 + T Cell Function by the Transcription Factor Eomesodermin

Author:

Pearce Erika L.12345,Mullen Alan C.12345,Martins Gislâine A.12345,Krawczyk Connie M.12345,Hutchins Anne S.12345,Zediak Valerie P.12345,Banica Monica12345,DiCioccio Catherine B.12345,Gross Darrick A.12345,Mao Chai-an12345,Shen Hao12345,Cereb Nezih12345,Yang Soo Y.12345,Lindsten Tullia12345,Rossant Janet12345,Hunter Christopher A.12345,Reiner Steven L.12345

Affiliation:

1. Abramson Family Cancer Research Institute, and Department of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.

2. Department of Microbiology, University of Pennsylvania, Philadelphia, PA 19104, USA.

3. Department of Pathobiology, University of Pennsylvania, Philadelphia, PA 19104, USA.

4. Samuel Lunenfeld Research Institute, and Mount Sinai Hospital, University of Toronto, Toronto, Ontario, Canada M5G 1X5.

5. Histogenetics, and Center for Genetic Polymorphism, Ossining, NY 10562, USA.

Abstract

Activated CD8 + T cells play a critical role in host defense against viruses, intracellular microbes, and tumors. It is not clear if a key regulatory transcription factor unites the effector functions of CD8 + T cells. We now show that Eomesodermin ( Eomes ), a paralogue of T-bet , is induced in effector CD8 + T cells in vitro and in vivo. Ectopic expression of Eomes was sufficient to invoke attributes of effector CD8 + T cells, including interferon-γ (IFN-γ), perforin, and granzyme B. Loss-of-function analysis suggests Eomes may also be necessary for full effector differentiation of CD8 + T cells. We suggest that Eomesodermin is likely to complement the actions of T-bet and act as a key regulatory gene in the development of cell-mediated immunity.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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