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Author Notes:
Corresponding authors: Ben Youngblood (benjamin.youngblood@stjude.org) and Rafi Ahmed (rahmed@emory.edu)
The authors declare that they have no disclosures.
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Research Funding:
This work was supported by National Institutes of Health (NIH) funding (R01 AI30048, P01 AI056299, and HHSN266200700006C) to Rafi Ahmed, NIH funding (F32 AI096709) to J. Scott Hale, and NIH funding (R01 AI114442) to Ben Youngblood.
Memory CD8 T cell transcriptional plasticity
Abstract:
Memory CD8 T cells generated after acute viral infections or live vaccines can persist for extended periods, in some instances for life, and play an important role in protective immunity. This long-lived immunity is achieved in part through cytokine-mediated homeostatic proliferation of memory T cells while maintaining the acquired capacity for rapid recall of effector cytokines and cytolytic molecules. The ability of memory CD8 T cells to retain their acquired properties, including their ability to remain poised to recall effector functions, is a truly impressive feat given that these acquired properties can be maintained for decades without exposure to cognate antigen. Here, we discuss general mechanisms for acquisition and maintenance of transcriptional programs in memory CD8 T cells and the potential role of epigenetic programming in maintaining the phenotypic and functional heterogeneity of cellular subsets among the pool of memory cells.
Copyright information:
© 2015 Faculty of 1000 Ltd
This is an Open Access article distributed under the terms of the Creative Commons Attribution 3.0 Unported License ( http://creativecommons.org/licenses/by/3.0/), which permits distribution of derivative works, distribution, public display, and publicly performance, making multiple copies, provided the original work is properly cited. This license requires copyright and license notices be kept intact, credit be given to copyright holder and/or author.
