Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Naturally occurring regulatory T (Treg) cells represent a distinct lineage of T lymphocytes that play a role in the regulation of immune responses and in the maintenance of peripheral tolerance. The discovery of Foxp3 as a key transcription factor selectively expressed in Treg cells enabled phenotypically defined populations of these cells to be identified and characterised. Here, we review the role of Foxp3 in the differentiation and function of Treg. Genetic Treg deficiency due to Foxp3-null mutations leads to systemic autoimmunity both in mice and humans. Earlier studies reported Foxp3 expression to be specific for Treg, designating Foxp3 as the 'regulatory T cell lineage specification factor'. However, recent observations challenge these views and implicate factors other than Foxp3 in Treg development. Whilst high and stable Foxp3 expression levels may be required to maintain the Treg cell phenotype and function, Treg lineage commitment might be independent of Foxp3. Further complexity is likely given the identification of novel Foxp3 splice variants in Treg cells; these may alter the functional outcomes of expression of this molecule. © 2009 Bentham Science Publishers Ltd.

Original publication

DOI

10.2174/157339509788166976

Type

Journal article

Journal

Current Immunology Reviews

Publication Date

18/08/2009

Volume

5

Pages

89 - 101