B7-Dc, a New Dendritic Cell Molecule with Potent Costimulatory Properties for T Cells

By S. Tseng, M. Otsuji, K. Gorski, Xin Huang, J. Slansky, S. Pai, A. Shalabi, T. Shin, D. Pardoll, H. Tsuchiya. Journal of Experimental Medicine, 2001

945 citations recorded by the source corpus.

Dendritic cells (DCs), unique antigen-presenting cells (APCs) with potent T cell stimulatory capacity, direct the activation and differentiation of T cells by providing costimulatory signals. As such, they are critical regulators of both natural and vaccine-induced immune responses. A new B7 family member, B7-DC, whose expression is highly restricted to DCs, was identified among a library of genes differentially expressed between DCs and activated macrophages. B7-DC fails to bind the B7.1/2 receptors CD28 and cytotoxic T lymphocyte–associated antigen (CTLA)-4, but does bind PD-1, a receptor for B7-H1/PD-L1. B7-DC costimulates T cell proliferation more efficiently than B7.1 and induces a distinct pattern of lymphokine secretion. In particular, B7-DC strongly costimulates interferon γ but not interleukin (IL)-4 or IL-10 production from isolated naive T cells. These properties of B7-DC may account for some of the unique activity of DCs, such as their ability to initiate potent T helper cell type 1 responses.

Subfields: Immunology, Oncology

View Paper: https://www.semanticscholar.org/paper/6757fe8dee2f8b6ac9a3385108b6a38d40558790

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

B7-H1 Expression on Non-Small Cell Lung Cancer Cells and Its Relationship with Tumor-Infiltrating Lymphocytes and Their PD-1 Expression (2004, background): “(33) reported that B7-DC costimulated T-cell proliferative responses and interferon production to greater levels than B7.”
Expression of Programmed Death 1 Ligands by Murine T Cells and APC1 (2002, neutral): “We previously observed that B7-DC mRNA was preferentially expressed in BMDCs (13).”
The Programmed Death-1 (PD-1) Pathway Regulates Autoimmune Diabetes in Nonobese Diabetic (NOD) Mice (2003, methodology): “Flow cytometry analysis showed that the anti–PD-1 mAb inhibited the binding of both PD-L1-Ig and PD-L2-Ig to PD-1 transfectants (Fig.”
Anti-PD-1/PD-L1 therapy of human cancer: past, present, and future. (2015, neutral): “In addition to PD-L1, another PD-1 ligand called B7-DC (also known as PD-L2) was also identified by the laboratories of Pardoll (9) and Freeman (10).”
The blockade of immune checkpoints in cancer immunotherapy (2012, background): “The two ligands for PD1 are PD1 ligand 1 (PDL1; also known as B7-H1 and CD274) and PDL2 (also known as B7-DC and CD273”
Interferon Receptor Signaling Pathways Regulating PD-L1 and PD-L2 Expression (2017, neutral): “PD-1 has two known ligands, PD-L1 (CD274 or B7-H1) and PD-L2 (CD273 or B7-DC), and both have been reported to be expressed on cell surfaces upon exposure to interferons, in particular interferon gamma (Kim et al., 2005; Dong et al., 2002; Tseng et al., 2001).”
Blockade of Programmed Death-1 Ligands on Dendritic Cells Enhances T Cell Activation and Cytokine Production 1 (2003, background): “(22) have reported that PD-L2-Ig (B7-DC-Ig) strongly costimulates T cell proliferation and enhances the secretion of IFN- .”
Mechanisms of immune evasion by tumors. (2006, background): “These ligands have very different tissue distribution patterns, wit B7‐DC expression is primarily confined to DCs and macrophages (Tseng et al., 2001).”
The function of programmed cell death 1 and its ligands in regulating autoimmunity and infection (2007, background): “, whereas others indicate that PD-1 ligands enhance T cell activatio”
PD-1 is a regulator of virus-specific CD8+ T cell survival in HIV infection (2006, background): “Although there is some evidence showing delivery of positive signals by the ligands of PD-1, programmed death ligand (PD-L)1 and PD-L2, (17, 18) the vast majority of the data point to negative regulation of T cell activation, proliferation, and cytokine production by these ligands (19–21).”