Epigenetic control in the immune response
Abramson Family Cancer Research Institute and Department of Medicine, Division of Infectious Diseases, University of Pennsylvania, Philadelphia, PA 19104, USA
* To whom correspondence should be addressed at: University of Pennsylvania, Building BRB II/III, Room 414, 421 Curie Boulevard, Philadelphia, PA 19104, USA. Tel: +1 2157465536; Fax: +1 2157465525; Email: sreiner{at}mail.med.upenn.edu
Received January 23, 2005; Accepted February 23, 2005
Helper T cells engaged in an immune response confront a prevalent challenge for developmentally regulated gene expression: How does a cell give rise to daughter cells with different fates? Additionally, lymphocyte function is intimately associated with the processes of cell division and migration. This imposes an additional burden for daughter cells, to remember inductive events from which they are temporally and spatially removed. An emerging view is that helper T cells use epigenetic mechanisms tied to the structure of chromatin and its covalent modifications to achieve at least two important features of their programed gene expression. Epigenetic effects organize the ability of signal transduction pathways to generate a restricted set of progeny from a multi-potent progenitor. In addition, epigenetic effects seem to allow dividing cells to memorize, or imprint, signaling events that occurred earlier in their development. Beyond helper T cells, the use of epigenetic effects is emerging as a common strategy in development and function of the mammalian immune system, suggesting that epigenetic effects may play a more prominent role in metazoan cell differentiation than previously appreciated. Lymphocytes are, thus, becoming a tractable system for genetic and biochemical dissection of the ways in which the genome is embedded with regulatory information to achieve developmental complexity.
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