https://transhumanist.ru/index.php?action=history&feed=atom&title=KIR2DL3KIR2DL3 - История изменений2026-04-08T02:55:01ZИстория изменений этой страницы в викиMediaWiki 1.43.6https://transhumanist.ru/index.php?title=KIR2DL3&diff=5328&oldid=prevOdysseusBot: Новая страница: «Killer cell immunoglobulin-like receptor 2DL3 precursor (CD158 antigen-like family member B2) (KIR-023GB) (Killer inhibitory receptor cl 2-3) (MHC class I NK cell...»2021-05-12T13:39:20Z<p>Новая страница: «Killer cell immunoglobulin-like receptor 2DL3 precursor (CD158 antigen-like family member B2) (KIR-023GB) (Killer inhibitory receptor cl 2-3) (MHC class I NK cell...»</p>
<p><b>Новая страница</b></p><div>Killer cell immunoglobulin-like receptor 2DL3 precursor (CD158 antigen-like family member B2) (KIR-023GB) (Killer inhibitory receptor cl 2-3) (MHC class I NK cell receptor) (NKAT2a) (NKAT2b) (Natural killer-associated transcript 2) (NKAT-2) (p58 natural killer cell receptor clone CL-6) (p58 NK receptor CL-6) (p58.2 MHC class-I-specific NK receptor) (CD158b2 antigen) [CD158B2] [KIRCL23] [NKAT2]<br />
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==Publications==<br />
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{{medline-entry<br />
|title=Epigenetic regulation of killer immunoglobulin-like receptor expression in T cells.<br />
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/19628706<br />
|abstract=With increasing age, T cells gain expression of killer immunoglobulin-like receptors (KIRs) that transmit negative signals and dampen the immune response. KIR expression is induced in [[CD4]] and CD8 T cells by CpG DNA demethylation suggesting epigenetic control. To define the mechanisms that underlie the age-associated preferential KIR expression in CD8 T cells, we examined [[KIR2DL3]] promoter methylation patterns. With age, CD8 T cells developed a patchy and stochastic promoter demethylation even in cells that did not express the [[KIR2DL3]]-encoded CD158b protein; complete demethylation of the minimal [[KIR2DL3]] promoter was characteristic for CD158b-expressing cells. In contrast, the promoter in [[CD4]] T cells was fully methylated irrespective of age. The selectivity for CD8 T cells correlated with lower [[DNMT1]] recruitment to the [[KIR2DL3]] promoter which further diminished with age. In contrast, binding of the polycomb protein [[EZH2]] known to be involved in [[DNMT1]] recruitment was not different. Our data suggest that CD8 T cells endure increasing displacement of [[DNMT1]] from the KIR promoter with age, possibly because of an active histone signature. The ensuing partial demethylation lowers the threshold for transcriptional activation and renders CD8 T cells more susceptible to express KIR, thereby contributing to the immune defect in the elderly.<br />
|mesh-terms=* Adult<br />
* Aged<br />
* Aged, 80 and over<br />
* Aging<br />
* CD4-Positive T-Lymphocytes<br />
* CD8-Positive T-Lymphocytes<br />
* CpG Islands<br />
* DNA (Cytosine-5-)-Methyltransferase 1<br />
* DNA (Cytosine-5-)-Methyltransferases<br />
* DNA Methylation<br />
* DNA-Binding Proteins<br />
* Enhancer of Zeste Homolog 2 Protein<br />
* Epigenesis, Genetic<br />
* Female<br />
* Humans<br />
* Male<br />
* Polycomb Repressive Complex 2<br />
* Promoter Regions, Genetic<br />
* Receptors, KIR2DL3<br />
* Transcription Factors<br />
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|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2765678<br />
}}</div>OdysseusBot