An article published last 27
December 2016 in “AGING CELL” using our Fixation/Permeabilization kit, by our customers from Department of Immunology, Hospital Universitario
Central de Asturias, Oviedo, Spain, in the study of Phenotypic characteristics
of aged CD4+ CD28null T
lymphocytes are determined by changes in the whole-genome DNA methylation
pattern. Congrats and Thanks.
Summary.
Aging is associated with a progressive loss of the CD28 costimulatory
molecule in CD4+ lymphocytes (CD28null T cells), which is accompanied by the
acquisition of new biological and functional properties that give rise to an
impaired immune response. The regulatory mechanisms that govern the appearance
and function of this cell subset during aging and in several associated
inflammatory disorders remain controversial. Here, we present the whole-genome
DNA methylation and gene expression profiles of CD28null T cells and its CD28+
counterpart. A comparative analysis revealed that 296 genes are differentially
methylated between the two cell subsets. A total of 160 genes associated with
cytotoxicity (e.g. GRZB, TYROBP, and RUNX3) and cytokine/chemokine signaling
(e.g. CX3CR1, CD27, and IL-1R) are demethylated in CD28null T cells, while 136
de novo-methylated genes matched defects in the TCR signaling pathway (e.g.
ITK, TXK, CD3G, and LCK). TCR-landscape analysis confirmed that CD28null T
cells have an oligo/monoclonal expansion over the polyclonal background of
CD28+ T cells, but feature a Vβ family repertoire specific to each individual. We reported that CD28null
T cells show a preactivation state characterized by a higher level of
expression of inflammasome-related genes that leads to the release of IL-1β when
activated. Overall, our results demonstrate that CD28null T cells have a unique
DNA methylation landscape, which is associated with differences in gene
expression, contributing to the functionality of these cells. Understanding
these epigenetic regulatory mechanisms could suggest novel therapeutic
strategies to prevent the accumulation and activation of these cells during
aging.
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