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	<id>https://transhumanist.ru/index.php?action=history&amp;feed=atom&amp;title=CD226</id>
	<title>CD226 - История изменений</title>
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	<updated>2026-06-23T18:22:54Z</updated>
	<subtitle>История изменений этой страницы в вики</subtitle>
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		<id>https://transhumanist.ru/index.php?title=CD226&amp;diff=6118&amp;oldid=prev</id>
		<title>OdysseusBot: Новая страница: «CD226 antigen precursor (DNAX accessory molecule 1) (DNAM-1) [DNAM1]  ==Publications==  {{medline-entry |title=T-cell Immunoglobulin and ITIM Domain Contributes t...»</title>
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		<updated>2021-05-12T15:12:38Z</updated>

		<summary type="html">&lt;p&gt;Новая страница: «CD226 antigen precursor (DNAX accessory molecule 1) (DNAM-1) [DNAM1]  ==Publications==  {{medline-entry |title=T-cell Immunoglobulin and ITIM Domain Contributes t...»&lt;/p&gt;
&lt;p&gt;&lt;b&gt;Новая страница&lt;/b&gt;&lt;/p&gt;&lt;div&gt;CD226 antigen precursor (DNAX accessory molecule 1) (DNAM-1) [DNAM1]&lt;br /&gt;
&lt;br /&gt;
==Publications==&lt;br /&gt;
&lt;br /&gt;
{{medline-entry&lt;br /&gt;
|title=T-cell Immunoglobulin and ITIM Domain Contributes to CD8  T-cell Immunosenescence.&lt;br /&gt;
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29349889&lt;br /&gt;
|abstract=Aging is associated with immune dysfunction, especially T-cell defects, which result in increased susceptibility to various diseases. Previous studies showed that T cells from aged mice express multiple inhibitory receptors, providing evidence of the relationship between T-cell exhaustion and T-cell senescence. In this study, we showed that T-cell immunoglobulin and immunoreceptor tyrosine-based inhibitory motif (ITIM) domain ([[TIGIT]]), a novel co-inhibitory receptor, was upregulated in CD8  T cells of elderly adults. Aged [[TIGIT]]  CD8  T cells expressed high levels of other inhibitory receptors including PD-1 and exhibited features of exhaustion such as downregulation of the key costimulatory receptor [[CD28]], representative intrinsic transcriptional regulation, low production of cytokines, and high susceptibility to apoptosis. Importantly, their functional defects associated with aging were reversed by [[TIGIT]] knockdown. [[CD226]] downregulation on aged [[TIGIT]]  CD8  T cells is likely involved in [[TIGIT]]-mediated negative immune suppression. Collectively, our findings indicated that [[TIGIT]] acts as a critical immune regulator during aging, providing a strong rationale for targeting [[TIGIT]] to improve dysfunction related to immune system aging.&lt;br /&gt;
|mesh-terms=* Adult&lt;br /&gt;
* Aged&lt;br /&gt;
* Animals&lt;br /&gt;
* CD8-Positive T-Lymphocytes&lt;br /&gt;
* Humans&lt;br /&gt;
* Immunoglobulins&lt;br /&gt;
* Immunosenescence&lt;br /&gt;
* Mice&lt;br /&gt;
* Middle Aged&lt;br /&gt;
* Receptors, Immunologic&lt;br /&gt;
|keywords=* &lt;br /&gt;
TIGIT&lt;br /&gt;
&lt;br /&gt;
* CD8  T cells&lt;br /&gt;
* T-cell immunosenescence&lt;br /&gt;
* aging&lt;br /&gt;
* co-inhibitory receptors&lt;br /&gt;
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5847879&lt;br /&gt;
}}&lt;/div&gt;</summary>
		<author><name>OdysseusBot</name></author>
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