Programmed death-1 ligand 1 interacts specifically with the B7-1 costimulatory molecule to inhibit T cell responses.

By M. Butte, M. Keir, T. Phamduy, Arlene H. Sharpe, G. Freeman. Immunity, 2007

1,664 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/bc7f8e2462ee6797b10e425273b11c40c41d4b32

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

In Oncology

Citations in the corpus

PD-L1 (B7-H1) and PD-1 Pathway Blockade for Cancer Therapy: Mechanisms, Response Biomarkers and Combinations (2016, background): “Activated T cells and APCs may express CD80, which may function as a receptor and deliver inhibitory signals when engaged by PD-L1 (42, 43).”
PD-1 and CTLA-4 combination blockade expands infiltrating T cells and reduces regulatory T and myeloid cells within B16 melanoma tumors (2010, background): “Recently, an additional coinhibitory ligand/receptor interaction has been described that involves binding of PD-L1 on T cells to B7-1 on APCs or vice versa (3).”
Immune checkpoint blockade: a common denominator approach to cancer therapy (2015, background): “An unexpected molecular interaction between PD-L1 and CD80 has been discovered (Butte et al., 2007; Park et al., 2010) whereby CD80 expressed on activated T cells (and possibly APCs) can function as a receptor rather than a ligand, delivering inhibitory signals when engaged by PD-L1.”
Tumor-associated macrophages: from mechanisms to therapy (2014, background): “…evidence from studies on the DC-T cell immunological synapse suggests that interaction of CTLA-4 with B7 ligands not only signals for the Immunity 41, July 17, 2014 ª2014 Elsevier Inc. 53 inhibition of T cells but also induces a DCs inhibitory phenotype (Butte et al., 2007; Mellor et al., 2004).”
Blockade of CTLA-4 on both effector and regulatory T cell compartments contributes to the antitumor activity of anti–CTLA-4 antibodies (2009, background): “After pan–T cell selection of cells derived from LN and spleen, purified populations of CD4+CD25+ T cells were mixed with the combined CD4+CD25 and CD8+ fractions (henceforth referred to as Teff) in four combinations to allow been revealed to be a specific binding partner of B7-1 with an affinity i”
Dual Blockade of PD-1 and CTLA-4 Combined with Tumor Vaccine Effectively Restores T Cell Rejection Function in Tumors (2013, background): “In contrast, aPD-L1 blocks both the PD-L1/PD-1 and the PD-L1/B7-1 inhibitory pathways but leaves the PD-1/PD-L2 inhibitory interaction unaffected (24, 25).”
Immune Checkpoint Blockade in Cancer Therapy. (2015, background): “In addition to binding PD-1, PD-L1 also is believed to exert negative signals on T cells by interacting with B7.”
Control of PD-L1 Expression by Oncogenic Activation of the AKT-mTOR Pathway in Non-Small Cell Lung Cancer. (2016, background): “PD-L1 binds to either PD-1 or CD80 receptors on activated immune cells to inhibit their activation and effector responses (8).”
T cell costimulatory receptor CD28 is a primary target for PD-1–mediated inhibition (2016, background): “Thus, during chronic viral infection, T cells become progressively “exhausted”, reflecting a homeostatic negative feedback loop due to increased expression of PD-1 and PD-L1(7-9).”
PD-1 regulates germinal center B cell survival and the formation and affinity of long-lived plasma cells (2010, background): “Although PD-1 has only two known ligands, PD-L1 and PD-L2, it has been shown that PD-L1 and CD80 interact to transduce bidirectional signal”