The PD-1-PD-L pathway in immunological tolerance.

By Taku Okazaki, Tasuku Honjo. Trends in immunology, 2006

744 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/a1eab38b54cbcc0bdf6e650ee9989772af672d79

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Citations in the corpus

Immune infiltration in human tumors: a prognostic factor that should not be ignored (2010, background): “, 2008), and T-cell-specific co-inhibitory molecules (CTLA-4 and PD-1) (Egen et al., 2002; Okazaki and Honjo, 2006).”
PD-1 Expression in Acute Hepatitis C Virus (HCV) Infection Is Associated with HCV-Specific CD8 Exhaustion (2006, background): “Many recent studies indicate that the PD-1/PD-1 ligand (PD-L1) pathway can play a role in T-cell exhaustion occurring when T cells are chronically exposed to high antigen loads and that blockade of PD-1/PDL-1 interaction can allow restoration of exhausted CD8 cells (1, 3, 4, 10, 12).”
Role of CXCR5 and CCR7 in Follicular Th Cell Positioning and Appearance of a Programmed Cell Death Gene-1High Germinal Center-Associated Subpopulation1 (2007, background): “Recent gene expression array studies identified additional genes that are up-regulated in CXCR5 T cells (7, 16, 17), including programmed cell death gene-1 (PD-1), a negative regulator of T cell activation (18).”
Plasmacytoid dendritic cells from mouse tumor-draining lymph nodes directly activate mature Tregs via indoleamine 2,3-dioxygenase. (2007, background): “because it has been found to mediate clonal exhaustion and T cell anergy in HIV and other chronic viral infections (34) as well as tolerance to self antigens and immune suppression in cancer (35).”
PD-1 signaling in primary T cells (2009, background): “In contrast to cytotoxic T-lymphocyte antigen-4 (CTLA-4) deficiency, which leads to a massive lymphoproliferative disorder within weeks of birth (7), PD-1 deficiency leads to species-specific autoimmunity that occurs much later in life (2).”
PD-1 is a regulator of virus-specific CD8+ T cell survival in HIV infection (2006, background): “Cross-linking of toll-like receptor (TLR)7 or 8 (with the TLR7/8 ligand Resiquimod) on mDCs substantially stimulated the expression of both PD-L1 and PD-L2 and caused a slight induction in PD-1 expression (Fig.”
Control of peripheral T‐cell tolerance and autoimmunity via the CTLA‐4 and PD‐1 pathways (2008, background): “PD-1-deficient mice, however, take several months to develop autoimmunity, and this disease is targeted to specific organs (43).”
The function of programmed cell death 1 and its ligands in regulating autoimmunity and infection (2007, background): “dtd" [ ]> The receptor 'programmed cell death 1' (PD-1; also called CD279) is inducibly expressed on CD4 + T cells, CD8 + T cells, natural killer T cells, B cells and activated monocyte”
Characterization of Hepatitis B Virus (HBV)-Specific T-Cell Dysfunction in Chronic HBV Infection (2007, background): “Recent studies indicate that exhausted T cells chronically exposed to high antigen loads express PD-1 (8, 14, 19, 23) and that the blocking of PD-1/PD-L1 engagement allows for the recovery of T-cell functions (1, 7, 23, 30, 32).”