Journal of immunology (Baltimore, Md. : 1950) · 2017
The Loss of TET2 Promotes CD8+ T Cell Memory Differentiation.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Carty Shannon A, Gohil Mercy, Banks Lauren B, Cotton Renee M, Johnson Matthew E, Stelekati Erietta, Wells Andrew D, Wherry E John, Koretzky Gary A, Jordan Martha S
Аннотация
T cell differentiation requires appropriate regulation of DNA methylation. In this article, we demonstrate that the methylcytosine dioxygenase ten-eleven translocation (TET)2 regulates CD8+ T cell differentiation. In a murine model of acute viral infection, TET2 loss promotes early acquisition of a memory CD8+ T cell fate in a cell-intrinsic manner without disrupting Ag-driven cell expansion or effector function. Upon secondary recall, TET2-deficient memory CD8+ T cells demonstrate superior pathogen control. Genome-wide methylation analysis identified a number of differentially methylated regions in TET2-deficient versus wild-type CD8+ T cells. These differentially methylated regions did not occur at the loci of differentially expressed memory markers; rather, several hypermethylated regions were identified in known transcriptional regulators of CD8+ T cell memory fate. Together, these data demonstrate that TET2 is an important regulator of CD8+ T cell fate decisions.
Предметные рубрики MeSH
AnimalsCD8-Positive T-LymphocytesCell DifferentiationCell ProliferationCells, CulturedDNA MethylationDNA-Binding ProteinsDioxygenasesImmunologic MemoryLymphocyte ActivationLymphocytic ChoriomeningitisLymphocytic choriomeningitis virusMiceMice, Inbred C57BLMice, KnockoutProto-Oncogene ProteinsT-Lymphocyte Subsets