Epigenetics mechanisms driving immune memory cell differentiation and function

A cardinal feature of adaptive T-cell responses to infection is the initiation of a largely autonomous differentiation program that results in proliferation and acquisition of lineage-specific T-cell functions. Moreover, upon clearance of infection, immunological memory is established whereby memory T cells retain the functional capacity acquired during the initial primary response. This enables pathogen specific T cells to respond more rapidly and robustly without the need for further differentiation. It has long been appreciated that changes in chromatin architecture and histone biochemical modifications play a role in the establishment of transcriptionally permissive structures at T-cell lineage effector gene loci. The advent of new technologies is now providing new insights into how epigenetic regulation not only impacts acquisition and maintenance of effector function, but also the maintenance of this functional capacity into memory, and how epigenetics regulates cell fate decisions that drive both effector and memory T-cell responses. This chapter will cover these topics.