PD-L1 and PD-L2 are differentially regulated by Th1 and Th2 cells

By P. Loke, James P. Allison. Proceedings of the National Academy of Sciences of the United States of America, 2003

636 citations recorded by the source corpus.

Subfields: Immunology, Oncology

View Paper: https://www.semanticscholar.org/paper/2d6bd2101d0ddf15d0662c3b39780c08eb520088

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In Immunology

1. Lieping Chen
2. R. Noy
3. A. Chawla
4. Antoni Ribas
5. P. Murray
6. B. Fife
7. T. Gajewski
8. Tasuku Honjo

In Oncology

1. Lieping Chen
2. Antoni Ribas
3. R. Noy
4. T. Gajewski
5. P. Murray
6. Janis Taube
7. Tasuku Honjo
8. C. Blank

Citations in the corpus

• Co-inhibitory molecules of the B7–CD28 family in the control of T-cell immunity (2004, background): “Interestingly, the expression of B7-H1 and B7-DC by macrophages could be differentially upregulated by T helper 1 (T H 1)- and T H 2-cell-derived cytokines, respectivel”
• Control of peripheral T‐cell tolerance and autoimmunity via the CTLA‐4 and PD‐1 pathways (2008, background): “PD-L1 is expressed on leukocytes, nonhematopoietic cells, and in non-lymphoid tissues including islets (21, 24, 25), while PD-L2 is expressed exclusively on DCs and monocytes (21, 22, 26, 27).”
• Alternative M2 activation of Kupffer cells by PPARdelta ameliorates obesity-induced insulin resistance. (2008, background): “As shown in Figure 2A, IL-4 failed to induce mRNAs encoding Retnla (resistin-like a), Mrc1 (mannose receptor), Chi3l3 (chitinase 3-like 3), and Pdcd1lg2 (programmed cell death 1 ligand 2) in PPARd / macrophages (Gordon, 2003; Loke and Allison, 2003; Raes et al., 2002).”
• PD-L1/B7H-1 Inhibits the Effector Phase of Tumor Rejection by T Cell Receptor (TCR) Transgenic CD8+ T Cells (2004, background): “A recent study has indicated that induction of PD-L2 on macrophages occurs with IL-4 treatment or interaction with Th2 cells (34), so it is possible that other cytokines could up-regulate PD-L2 expression on tumor cells.”
• Tumor-associated macrophages: from mechanisms to therapy (2014, background): “For example, it has been shown that INF-g secretion by activated NK cells that have migrated to the lymph node is an important mediator of CD8+ T cell activation and that HLA-G and HLA-E inhibits this NK cells migration and INF-g secretion (Kelly et al., 2002).”
• 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): “Of note, PD-L1 expression was also found on naı̈ve cells and up-regulated on activated T cells [37].”
• Control of PD-L1 Expression by Oncogenic Activation of the AKT-mTOR Pathway in Non-Small Cell Lung Cancer. (2016, background): “In DCs, LPS and IFNgmediated induction of PD-L1 protein depends on both active transcription and translation (38).”
• Interferon Receptor Signaling Pathways Regulating PD-L1 and PD-L2 Expression (2017, positive): “Evidence has been generated for the role of STAT1 and STAT3, as well as the downstream transcription factor IRF1, in regulating the surface expression of PD-L1 upon interferon gamma exposure (Lee et al., 2006; Loke and Allison, 2003).”
• PD-1 and its ligands in tolerance and immunity. (2008, neutral): “Blockade of programmed death-1 engagement accelerates graft-versus-host disease lethality by an IFN-γ-dependent mechanism.”
• Oxidative metabolism and PGC-1beta attenuate macrophage-mediated inflammation. (2006, result): “Flow cytometric analyses of these and other alternative activation makers (Gordon, 2003;Loke and Allison, 2003) further supported this conclusion (Figures S2A–S2C).”