Редактирование: CD226 (раздел)

==Publications==

{{medline-entry
|title=T-cell Immunoglobulin and ITIM Domain Contributes to CD8  T-cell Immunosenescence.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29349889
|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.
|mesh-terms=* Adult
* Aged
* Animals
* CD8-Positive T-Lymphocytes
* Humans
* Immunoglobulins
* Immunosenescence
* Mice
* Middle Aged
* Receptors, Immunologic
|keywords=* 
TIGIT

* CD8  T cells
* T-cell immunosenescence
* aging
* co-inhibitory receptors
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5847879
}}