Редактирование: CD3G

T-cell surface glycoprotein CD3 gamma chain precursor (T-cell receptor T3 gamma chain) (CD3g antigen) [T3G]

==Publications==

{{medline-entry
|title=Phenotypic characteristics of aged [[CD4]]  [[CD28]]  T lymphocytes are determined by changes in the whole-genome DNA methylation pattern.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/28026094
|abstract=Aging is associated with a progressive loss of the [[CD28]] costimulatory molecule in [[CD4]]  lymphocytes ([[CD28]]  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 [[CD28]]  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 [[CD28]]  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 [[CD28]]  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 [[CD28]]  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 [[CD28]]  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.
|mesh-terms=* Apoptosis
* CD28 Antigens
* CD4 Antigens
* CD4-Positive T-Lymphocytes
* Cellular Senescence
* CpG Islands
* Cytotoxicity, Immunologic
* DNA Methylation
* Gene Expression Regulation
* Genome, Human
* Humans
* Immunity
* Inflammasomes
* Phenotype
* Receptors, Antigen, T-Cell
* Reproducibility of Results
* Signal Transduction
|keywords=* CD4  CD28null T cells
* DNA methylation
* TCR signaling
* aging
* gene expression
* inflammation
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5334526
}}