The B7 family revisited.
By R. Greenwald, G. Freeman, Arlene H. Sharpe. Annual Review of Immunology, 2005
2,575 citations recorded by the source corpus.
Subfields: Immunology, Oncology
View Paper: https://www.semanticscholar.org/paper/ae7f02d2e4e2e2692d7244dfa252b6a5a2e65d1b
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Immunology
- E. Wherry
- Rafi Ahmed
- Lieping Chen
- D. Pardoll
- Arlene H. Sharpe
- G. Freeman
- James L. Riley
- James P. Allison
In Oncology
- Lieping Chen
- D. Pardoll
- E. Wherry
- Arlene H. Sharpe
- James P. Allison
- G. Freeman
- Rafi Ahmed
- James L. Riley
Citations in the corpus
- 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”
- The blockade of immune checkpoints in cancer immunotherapy (2012, background): “In the case of T cells, the ultimate amplitude and quality of the response, which is initiated through antigen recognition by the T cell receptor (TCR), is regulated by a balance between co-stimulatory and inhibitory signals (that is, immune checkpoints”
- Combining Immunotherapy and Targeted Therapies in Cancer Treatment (2012, background): “Second, tumour-specific T cells must differentiate into effector T cells, which requires a combination of signals from both the T cell receptor (TCR) — which establishes specificity — and several co-stimulatory molecule”
- Tumor-infiltrating NY-ESO-1–specific CD8+ T cells are negatively regulated by LAG-3 and PD-1 in human ovarian cancer (2010, background): “In this regard, programmed cell death-1 (PD-1, CD279), an immune inhibitory receptor belonging to the CD28:B7 family of costimulatory molecules, which is expressed on activated T cells, B cells, and myeloid cells (8), may play a role in downregulating tumor immunity in EOC.”
- The B7-H1 (PD-L1) T lymphocyte-inhibitory molecule is expressed in breast cancer patients with infiltrating ductal carcinoma: correlation with important high-risk prognostic factors. (2006, methodology): “previously described by Greenwald et al. [ 42 ].”
- Universal Chimeric Antigen Receptors for Multiplexed and Logical Control of T Cell Responses (2018, neutral): “However, the repertoire of co-signaling domains—both co-stimulatory and co-inhibitory domains—are highly diverse, and it is the activation of different co-signaling domains that sculpts ultimate T cell function (Chen and Flies, 2013; Greenwald et al., 2005; Zhu et al., 2011).”
- CTLA-4 and PD-1 Pathways (2016, background): “Central to this process are the cytotoxic T-lymphocyte–associated antigen 4 (CTLA-4) and programmed death 1 (PD-1) immune checkpoint pathways.(3) The CTLA-4 and PD-1 pathways are thought to operate at different stages of an immune response.”
- The surface protein TIGIT suppresses T cell activation by promoting the generation of mature immunoregulatory dendritic cells (2009, background): “CD28 and the T cell inhibitory receptor CTLA-4 on T cells interact with B7 molecules on DCs and costimulate and coinhibit T cell activation, respectivel”