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Foxp3-dependent programme of regulatory T-cell differentiation

Foxp3-dependent programme of regulatory T-cell differentiation Regulatory CD4+ T cells (T r cells), the development of which is critically dependent on X-linked transcription factor Foxp3 (forkhead box P3), prevent self-destructive immune responses 1 . Despite its important role, molecular and functional features conferred by Foxp3 to T r precursor cells remain unknown. It has been suggested that Foxp3 expression is required for both survival of T r precursors as well as their inability to produce interleukin (IL)-2 and independently proliferate after T-cell-receptor engagement, raising the possibility that such ‘anergy’ and T r suppressive capacity are intimately linked 2,3,4 . Here we show, by dissociating Foxp3-dependent features from those induced by the signals preceding and promoting its expression in mice, that the latter signals include several functional and transcriptional hallmarks of T r cells. Although its function is required for T r cell suppressor activity, Foxp3 to a large extent amplifies and fixes pre-established molecular features of T r cells, including anergy and dependence on paracrine IL-2. Furthermore, Foxp3 solidifies T r cell lineage stability through modification of cell surface and signalling molecules, resulting in adaptation to the signals required to induce and maintain T r cells. This adaptation includes Foxp3-dependent repression of cyclic nucleotide phosphodiesterase 3B, affecting genes responsible for T r cell homeostasis. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Nature Springer Journals

Foxp3-dependent programme of regulatory T-cell differentiation

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References (26)

Publisher
Springer Journals
Copyright
Copyright © 2006 by Nature Publishing Group
Subject
Science, Humanities and Social Sciences, multidisciplinary; Science, Humanities and Social Sciences, multidisciplinary; Science, multidisciplinary
ISSN
0028-0836
eISSN
1476-4687
DOI
10.1038/nature05543
Publisher site
See Article on Publisher Site

Abstract

Regulatory CD4+ T cells (T r cells), the development of which is critically dependent on X-linked transcription factor Foxp3 (forkhead box P3), prevent self-destructive immune responses 1 . Despite its important role, molecular and functional features conferred by Foxp3 to T r precursor cells remain unknown. It has been suggested that Foxp3 expression is required for both survival of T r precursors as well as their inability to produce interleukin (IL)-2 and independently proliferate after T-cell-receptor engagement, raising the possibility that such ‘anergy’ and T r suppressive capacity are intimately linked 2,3,4 . Here we show, by dissociating Foxp3-dependent features from those induced by the signals preceding and promoting its expression in mice, that the latter signals include several functional and transcriptional hallmarks of T r cells. Although its function is required for T r cell suppressor activity, Foxp3 to a large extent amplifies and fixes pre-established molecular features of T r cells, including anergy and dependence on paracrine IL-2. Furthermore, Foxp3 solidifies T r cell lineage stability through modification of cell surface and signalling molecules, resulting in adaptation to the signals required to induce and maintain T r cells. This adaptation includes Foxp3-dependent repression of cyclic nucleotide phosphodiesterase 3B, affecting genes responsible for T r cell homeostasis.

Journal

Nature – Springer Journals

Published: Jan 14, 2007

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