Matches in SemOpenAlex for { <https://semopenalex.org/work/W4297260156> ?p ?o ?g. }
- W4297260156 abstract "Cellular senescence is a stable form of cell cycle arrest associated with proinflammatory responses. Senescent cells can be cleared by the immune system as a part of normal tissue homeostasis. However, senescent cells can also accumulate in aged and diseased tissues, contributing to inflammation and disease progression. The mechanisms mediating the impaired immune-mediated clearance of senescent cells are poorly understood. Here, we report that senescent cells upregulate the immune checkpoint molecule PD-L1, the ligand for PD-1 on immune cells, which drives immune cell inactivation. The induction of PD-L1 in senescence is dependent on the proinflammatory program. Furthermore, the secreted factors released by senescent cells are sufficient to upregulate PD-L1 in nonsenescent control cells, mediated by the JAK-STAT pathway. In addition, we show that prolongevity intervention rapamycin downregulates PD-L1 in senescent cells. Last, we found that PD-L1 is upregulated in several tissues in naturally aged mice and in the lungs of idiopathic pulmonary fibrosis patients. Together, our results report that senescence and aging are associated with upregulation of a major immune checkpoint molecule, PD-L1. Targeting PD-L1 may offer new therapeutic opportunities in treating senescence and age-associated diseases." @default.
- W4297260156 created "2022-09-28" @default.
- W4297260156 creator A5002832519 @default.
- W4297260156 creator A5004377642 @default.
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- W4297260156 date "2022-10-01" @default.
- W4297260156 modified "2023-10-16" @default.
- W4297260156 title "Upregulation of PD-L1 in Senescence and Aging" @default.
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- W4297260156 doi "https://doi.org/10.1128/mcb.00171-22" @default.
- W4297260156 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/36154662" @default.
- W4297260156 hasPublicationYear "2022" @default.
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