PD‐1:PD‐L inhibitory pathway affects both CD4+ and CD8+ T cells and is overcome by IL‐2
By L. Carter, L. Fouser, J. Jussif, L. Fitz, Bija Deng, C. Wood, M. Collins, Tasuku Honjo, G. Freeman, B. Carreno. European Journal of Immunology, 2002
721 citations recorded by the source corpus.
Subfields: Immunology, Oncology
View Paper: https://www.semanticscholar.org/paper/81c4998223e1e169723994ea19f2c997c5878695
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Citations in the corpus
- SHP-1 and SHP-2 Associate with Immunoreceptor Tyrosine-Based Switch Motif of Programmed Death 1 upon Primary Human T Cell Stimulation, but Only Receptor Ligation Prevents T Cell Activation1 (2004, background): “Others have shown that PD-1 expression is up-regulated after B and T cell activation, and that maximal expression is observed after 48 h (10, 37, 38).”
- PD-1 signaling in primary T cells (2009, background): “The importance of targeting Akt and glucose metabolism by negative regulators of T-cell activation is underscored by the observations that IL-2 can override the effects of PD-1 ligation (44).”
- Expression of Programmed Death 1 Ligands by Murine T Cells and APC1 (2002, background): “The engagement of PD-1 by B7-H1 or B7-DC has been reported to inhibit TCR/CD3-mediated T cell proliferation and cytokine production (11, 12, 17).”
- Interaction of PD-L1 on tumor cells with PD-1 on tumor-specific T cells as a mechanism of immune evasion: implications for tumor immunotherapy (2005, background): “The fact that PD-L1/PD-1 engagement can attenuate ICOS-positive costimulatory signals [5], that its negative signaling however can be negated by CD28 ligation or IL-2 [12], and the identification of a further negative regulatory receptor, BTLA [11, 75], indicates that the overall result from negativ”
- PD-1 and its ligands in tolerance and immunity. (2008, background): “This reduction can be overcome by costimulation through CD28 (8) or IL-2 (33).”
- Blockade of Programmed Death-1 Ligands on Dendritic Cells Enhances T Cell Activation and Cytokine Production 1 (2003, background): “(12) have shown that PD-Ls inhibit CD8 T cell activation more effectively than CD4 T cell activation, and Iwai et al.”
- Anti-PD-1 and Anti-CTLA-4 Therapies in Cancer: Mechanisms of Action, Efficacy, and Limitations (2018, background): “By interfering with early TCR/CD28 signaling and associated IL-2-dependent positive feedback, PD-1 signaling therefore results in reduced cytokine production [such as IL-2, IFN-γ, and tumor necrosis factor (TNF)-α], cell cycle progression, and pro-survival Bcl-xL gene expression, as well as reduced ”
- Control of peripheral T‐cell tolerance and autoimmunity via the CTLA‐4 and PD‐1 pathways (2008, background): “Further studies have shown that PD-1 is more likely to function on cellular activation and not directly on death (55, 56).”