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dc.contributor.authorAttridge, Kesley
dc.contributor.authorWalker, LSK
dc.date.accessioned2019-07-01T10:44:08Z
dc.date.available2019-07-01T10:44:08Z
dc.date.issued2014-01-01
dc.identifier.citationAttridge, K. and Walker, L. S. K. (2014) Homeostasis and function of regulatory T cells (Tregs) in vivo: Lessons from TCR-transgenic Tregs, Immunological Reviews, 259 (2014), pp. 23-39.en
dc.identifier.issn0105-2896en
dc.identifier.pmid24712457
dc.identifier.doi10.1111/imr.12165en
dc.identifier.urihttp://hdl.handle.net/2436/622490
dc.description.abstractThe identification of CD25 and subsequently Forkhead box protein 3 (Foxp3) as markers for regulatory T cells (Tregs) has revolutionized our ability to explore this population experimentally. In a similar vein, our understanding of antigen-specific Treg responses in vivo owes much to the fortuitous generation of T-cell receptor (TCR)-transgenic Tregs. This has permitted tracking of Tregs with a defined specificity in vivo, facilitating analysis of how encounter with cognate antigen shapes Treg homeostasis and function. Here, we review the key lessons learned from a decade of analysis of TCR-transgenic Tregs and set this in the broader context of general progress in the field. Use of TCR-transgenic Tregs has led to an appreciation that Tregs are a highly dynamic proliferative population in vivo, rather than an anergic population as they were initially portrayed. It is now clear that Treg homeostasis is positively regulated by encounter with self-antigen expressed on peripheral tissues, which is likely to be relevant to the phenomenon of peripheral repertoire reshaping that has been described for Tregs and the observation that the Treg TCR specificities vary by anatomical location. Substantial evidence has also accumulated to support the role of CD28 costimulation and interleukin-2 in Treg homeostasis. The availability of TCR-transgenic Tregs has enabled analysis of Treg populations that are sufficient or deficient in particular genes, without the comparison being confounded by repertoire alterations. This approach has yielded insights into genes required for Treg function in vivo, with particular progress being made on the role of ctla-4 in this context. As the prospect of manipulating Treg populations in the clinic becomes reality, a full appreciation of the rules governing their homeostasis will prove increasingly important. © 2014 The Authors. Immunological Reviews Published by John Wiley & Sons Ltd.en
dc.formatapplication/PDFen
dc.languageeng
dc.language.isoenen
dc.publisherWileyen
dc.relation.urlhttps://onlinelibrary.wiley.com/doi/full/10.1111/imr.12165en
dc.rightsLicence for published version: Creative Commons Attribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectThymus Glanden
dc.subjectAnimalsen
dc.subjectHumansen
dc.subjectReceptors, Antigen, T-Cellen
dc.subjectLymphocyte Activationen
dc.subjectSignal Transductionen
dc.subjectImmune Toleranceen
dc.subjectHomeostasisen
dc.subjectT-Lymphocytes, Regulatoryen
dc.subjectClonal Selection, Antigen-Mediateden
dc.titleHomeostasis and function of regulatory T cells (Tregs) in vivo: Lessons from TCR-transgenic Tregsen
dc.typeJournal articleen
dc.identifier.eissn1600-065X
dc.identifier.journalImmunological Reviewsen
dc.date.updated2019-06-20T16:11:27Z
dc.contributor.institutionKennedy Institute of Rheumatology, University of Oxford, Oxford, UK.
pubs.place-of-publicationEngland
rioxxterms.identifier.projectG0802382en
rioxxterms.versionVoRen
rioxxterms.licenseref.urihttp://creativecommons.org/licenses/by/4.0/en
rioxxterms.licenseref.startdate2019-07-01en
dc.source.volume259
dc.source.issue1
dc.source.beginpage23
dc.source.endpage39
dc.description.versionPublished version
refterms.dateFCD2019-07-01T10:43:27Z
refterms.versionFCDVoR
refterms.dateFOA2019-07-01T10:44:08Z


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Licence for published version: Creative Commons Attribution 4.0 International
Except where otherwise noted, this item's license is described as Licence for published version: Creative Commons Attribution 4.0 International