Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 116, Issue 10, Pages 4471-4480Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1800494116
Keywords
E protein; effector Treg cell; TCR signaling; gene regulatory network; differentiation and function
Categories
Funding
- Strategic Priority Research Program of the Chinese Academy of Sciences [XDB29010000]
- National Natural Science Foundation of China [31670894]
- National Key Research and Development Project of China [2016YFC1200302]
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [ZIAAI000354, ZIAAI000872] Funding Source: NIH RePORTER
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T cell antigen receptor (TCR) signaling is essential for the differentiation and maintenance of effector regulatory T (Treg) cells. However, the contribution of individual TCR-dependent genes in Treg cells to the maintenance of immunotolerance remains largely unknown. Here we demonstrate that Treg cells lacking E protein undergo further differentiation into effector cells that exhibit high expression of effector Treg signature genes, including IRF4, ICOS, CD103, KLRG-1, and ROR gamma t. E protein-deficient Treg cells displayed increased stability and enhanced suppressive capacity. Transcriptome and ChIP-seq analyses revealed that E protein directly regulates a large proportion of the genes that are specific to effector Treg cell activation, and importantly, most of the up-regulated genes in E protein-deficient Treg cells are also TCR dependent; this indicates that E proteins comprise a critical gene regulatory network that links TCR signaling to the control of effector Treg cell differentiation and function.
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