NDLI: IL-2R signaling is essential for functional maturation of T regulatory cells during thymic development 1

Content Provider	PubMed Central
Author	Cheng, Guoyan Yu, Aixin Dee, Michael J. Malek, Thomas R.
Abstract	CD4+ Foxp3+ Tregs are an independent cell lineage and their developmental progression during thymic development depends on IL-2R signaling. However, the role of IL-2R signaling during thymic Treg development remains only partially understood. The current study assessed the contribution of IL-2 in the expansion and functional programming of developing Tregs. In the absence of IL-2Rβ signaling, predominately CD4+ CD25- Foxp3lo T cells were found and these cells exhibited somewhat lower expression of the proliferative marker Ki67. These immature Tregs, which represent products of failed development, were also found in normal mice and characterized by markedly lower expression of several Treg functional molecules. IL-2R signaling, therefore, is required for the progression, functional programming, and expansion of Tregs during thymic development. An IL-2R signaling mutant that lowers STAT5 activation readily supported Treg functional programming but Treg proliferation remained somewhat impaired. The requirement for IL-2 during thymic Treg expansion was best illustrated in mixed chimeras where the Tregs with mutant IL-2Rs were forced to compete with WT Tregs during their development. Tregs with impaired IL-2R signaling were more prevalent in the thymus than spleen in these competitive experiments. The general effectiveness of mutant IL-2Rs to support thymic Treg development is partially accounted for by a heighten capacity of thymic Tregs to respond to IL-2. Overall our data support a model where limiting IL-2R signaling is amplified by thymic Tregs to readily support their development and functional programming whereas these same conditions are not sufficient to support peripheral Treg homeostasis.
Related Links	http://dx.doi.org/10.4049/jimmunol.1201218
Ending Page	1575
Page Count	9
Starting Page	1567
File Format	PDF
ISSN	00221767
e-ISSN	15506606
Journal	Journal of immunology (Baltimore, Md. : 1950)
Issue Number	4
Volume Number	190
Language	English
Publisher Date	2013-02-15
Access Restriction	Open
Subject Keyword	Medicine(all) Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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