Key Product Details

Species Reactivity

Mouse

Applications

Immunohistochemistry

Label

DyLight 350 (Excitation = 353 nm, Emission = 432 nm)

Antibody Source

Recombinant Monoclonal Rabbit IgG Clone # 2096A
View all PD-L1/B7-H1 Primary Antibodies »

Product Specifications

Immunogen

Mouse myeloma cell line, NS0 derived mouse PD-L1/B7-H1
Phe19-His239
Accession # Q9EP73

Specificity

Detects recombinant mouse PD-L1 protein in Direct ELISA.

Clonality

Monoclonal

Host

Rabbit

Isotype

IgG

Applications for PD-L1 Antibody (2096A) [Dylight 350]

Application
Recommended Usage

Immunohistochemistry

Optimal dilutions of this antibody should be experimentally determined.
Application Notes
Optimal dilution of this antibody should be experimentally determined.

Formulation, Preparation, and Storage

Purification

Protein A or G purified from cell culture supernatant

Formulation

50mM Sodium Borate

Preservative

0.05% Sodium Azide

Concentration

Please see the vial label for concentration. If unlisted please contact technical services.

Shipping

The product is shipped with polar packs. Upon receipt, store it immediately at the temperature recommended below.

Stability & Storage

Store at 4C in the dark.

Background: PD-L1/B7-H1

Programmed-death ligand 1 (PD-L1), also known as CD274 and B7-H1, is a 33 kDa type I glycoprotein containing 290 amino acids (aa) belonging to the protein B7 family and serves as part of an immune checkpoint (1,2). PD-L1 contains an Ig-V and Ig-C-like extracellular domain, a transmembrane domain, and a cytoplasmic tail lacking canonical signaling motifs (2,3). PD-L1 is the ligand that binds the receptor programmed-death 1 (PD-1) which is highly expressed on active T cells (1-3). PD-L1 is typically upregulated by tumor cells and antigen presenting cells (APCs), but also expressed on T cells, B cells, macrophages, dendritic cells (DC), mast cells, and some non-immune cell types (1-3). In addition to the membrane-bound, PD-L1 is released from cells both in soluble form and bound to extracellular vesicles (4).

PD-L1 binding with receptor PD-1 results in phosphorylation of in the inhibitory tyrosine-based switch motif (ITSM) domain of PD-1, which leads to recruitment of Src homology 2 domain-containing protein tyrosine-phosphatase 2 (SHP-2) and eventual downstream phosphorylation of spleen tyrosine kinase (Syk) and phospholipid inositol-3-kinase (PI3K) (1,3). Under normal conditions, the PD-L1/PD-1 signaling axis helps maintain immune tolerance and prevent destructive immune responses by inhibiting T cell activity such as proliferation, survival, cytokine production, and cytotoxic T lymphocyte (CTL) cytotoxicity (1-3). In the tumor microenvironment (TME), however, the PD-L1/PD-1 signaling axis is hijacked to promote tumor cell survival and limit anti-tumor immune response (1,3). More precisely, tumor cells can escape killing and immune surveillance due to T cell exhaustion and apoptosis (1-3).

Given the role the PD-L1/PD-1 signaling axis plays in tumor cells' ability to evade immune surveillance, it has become a target of several immunotherapeutic agents in recent years (3,5). Antibody immunotherapies that target these inhibitory checkpoint molecules has shown great promise for cancer treatment (3,5). PD-L1 and PD-1 blocking agents have been approved for treatment in a number of cancers including melanoma, non-small cell lung cancer (NSCLC), urothelial carcinoma, and Merkel-cell carcinoma (3,5). In many cancers the expression of PD-L1 in the TME has predictive value for response to blocking agents (3). Pembrolizumab, for example, is a PD-1 inhibitor that has been approved by the FDA as a second-line therapy for treatment of metastatic NSCLC in patients whose tumors express PD-L1 with a Tumor Proportion Score (TPS) greater than 1%, but also for first-line treatment in cases where patients' tumors expression PD-L1 with a TPS greater than 50%) (5). The most promising cancer immunotherapy treatments seem to point to combination therapy with both anti-cancer drugs (e.g. Gefitibin, Metformin, Etoposide) with PD-L1/PD-1 antibody blockade inhibitors (e.g. Atezolizumab, Nivolumab) (6).

References

1. Han, Y., Liu, D., & Li, L. (2020). PD-1/PD-L1 pathway: current researches in cancer. American journal of cancer research, 10(3), 727-742.

2. Jiang, Y., Chen, M., Nie, H., & Yuan, Y. (2019). PD-1 and PD-L1 in cancer immunotherapy: clinical implications and future considerations. Human vaccines & immunotherapeutics, 15(5), 1111-1122. https://doi.org/10.1080/21645515.2019.1571892

3. Sun, C., Mezzadra, R., & Schumacher, T. N. (2018). Regulation and Function of the PD-L1 Checkpoint. Immunity, 48(3), 434-452. https://doi.org/10.1016/j.immuni.2018.03.014

4. Cha, J. H., Chan, L. C., Li, C. W., Hsu, J. L., & Hung, M. C. (2019). Mechanisms Controlling PD-L1 Expression in Cancer. Molecular cell, 76(3), 359-370. https://doi.org/10.1016/j.molcel.2019.09.030

5. Tsoukalas, N., Kiakou, M., Tsapakidis, K., Tolia, M., Aravantinou-Fatorou, E., Baxevanos, P., Kyrgias, G., & Theocharis, S. (2019). PD-1 and PD-L1 as immunotherapy targets and biomarkers in non-small cell lung cancer. Journal of B.U.ON. : official journal of the Balkan Union of Oncology, 24(3), 883-888.

6. Gou, Q., Dong, C., Xu, H., Khan, B., Jin, J., Liu, Q., Shi, J., & Hou, Y. (2020). PD-L1 degradation pathway and immunotherapy for cancer. Cell death & disease, 11(11), 955. https://doi.org/10.1038/s41419-020-03140-2

Long Name

Programmed Death Ligand 1

Alternate Names

B7-H1, B7H1, CD274, PDCD1L1, PDCD1LG1, PDL1

Additional PD-L1/B7-H1 Products

Product Documents for PD-L1 Antibody (2096A) [Dylight 350]

Certificate of Analysis

To download a Certificate of Analysis, please enter a lot or batch number in the search box below.

Download SDS

Product Specific Notices for PD-L1 Antibody (2096A) [Dylight 350]



DyLight (R) is a trademark of Thermo Fisher Scientific Inc. and its subsidiaries.

This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.

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Protocols

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