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- W2898677536 abstract "Abstract Programmed death (PD)-1 receptors and their ligands have been identified in the pathogenesis and development of systemic lupus erythematosus (SLE). Two key pathways, toll-like receptor and type I interferon, are significant to SLE pathogenesis and modulate the expression of PD-1 and the ligands (PD-L1, PD-L2) through activation of NF-κB and/or STAT1. These cell signals are regulated by tyrosine kinase (Tyro, Axl, Mer) receptors (TAMs) that are aberrantly activated in SLE. STAT1 and NF-κB also exhibit crosstalk with the aryl hydrocarbon receptor (AHR). Ligands to AHR are identified in SLE etiology and pathogenesis. These ligands also regulate the activity of the Epstein-Barr virus (EBV), which is an identified factor in SLE and PD-1 immunobiology. AHR is important in the maintenance of immune tolerance and the development of distinct immune subsets, highlighting a potential role of AHR in PD-1 immunobiology. Understanding the functions of AHR ligands as well as AHR crosstalk with STAT1, NF-κB, and EBV may provide insight into disease development, the PD-1 axis and immunotherapies that target PD-1 and its ligand, PD-L1." @default.
- W2898677536 created "2018-11-09" @default.
- W2898677536 creator A5001418105 @default.
- W2898677536 creator A5019048294 @default.
- W2898677536 creator A5022594161 @default.
- W2898677536 creator A5081582773 @default.
- W2898677536 date "2019-02-01" @default.
- W2898677536 modified "2023-10-03" @default.
- W2898677536 title "PD-1 immunobiology in systemic lupus erythematosus" @default.
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