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Typically, during viral infections, T cells encounter antigen, undergo proliferative expansion and ultimately contract into a pool of memory cells. However, after infection with cytomegalovirus, a ubiquitous β-herpesvirus, T cell populations specific for certain epitopes do not contract but instead are maintained and/or accumulate at high frequencies with a characteristic effector-memory phenotype. This feature has also been noted after other infections, for example, by parvoviruses. We discuss this so-called memory T cell inflation and the factors involved in this phenomenon. Also, we consider the potential therapeutic use of memory T cell inflation as a vaccine strategy and the associated implications for immune senescence. © 2011 Elsevier Ltd.

Original publication

DOI

10.1016/j.it.2011.11.005

Type

Journal article

Journal

Trends in Immunology

Publication Date

01/02/2012

Volume

33

Pages

84 - 90