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Immuno-oncology has revolutionized the way we treat cancer. Cell therapy and immune checkpoint inhibitor therapy can lead to durable cancer remission. Immune checkpoint inhibitor therapy removes the inhibitory signals of T cell activation, allowing the immune system to mount an effective anti-tumor response.1 Antibodies against Cytotoxic T-Lymphocyte Antigen 4 (CTLA-4), Programmed Death-1 (PD-1), and Programmed Death Ligand-1 (PD-L1) successfully treat many cancers, including melanomas, carcinomas, and non-small cell lung cancer. Immunoassays provide a tool for researchers to gain additional insights for developing treatment options for cancers and autoimmune diseases. Their ability to provide precise and highly sensitive results allows researchers to quantitatively assess the presence and abundance of disease markers, shedding light on the disease's progression and severity.
Immune Checkpoint ELISA Kits
R&D Systems immune checkpoint immunoassays are sensitive, specific, and provide high-quality data so you don’t have to worry about repeating experiments. We have decades of experience manufacturing immunoassays. Count on our immunoassays for consistent and reproducible data. Our immunoassays are regularly tested for lot-to-lot consistency, precision, recovery, and linearity.
Which Immunoassay Best Suits my Needs
Choose R&D Systems™ Luminex® assays to maximize multiplexing capacity and flexibility while maintaining specificity. Leverage Quantikine™ ELISAs, the most trusted name in the market to for accurate and reproducible results. QuicKit ELISAs offer Quantikine-quality data in 90 minutes or less. DuoSet ELISAs are a cost-effect alternative to buying separate antibodies and proteins and optimizing your own assay. Learn more about R&D Systems different ELISA Kit formats.
CTLA-4
Cytotoxic T-Lymphocyte Antigen-4 (CTLA-4) plays a well-described immunosuppressive role in the immune system, specifically in the interaction between T cells and antigen-presenting cells (APCs).1 CTLA-4 keeps immune responses within a desired physiological range to protect against autoimmunity. CTLA-4 expression at the immunological synapse is upregulated in response to T Cell Receptor (TCR) stimulation, peaking at 2-3 days. It has a higher affinity and is a more avid receptor for B7-1 and B7-2 than the co-stimulatory CD28 receptor. By outcompeting CD28, CTLA-4 diminishes TCR signaling and attenuates T cell activation. Tumors take advantage of the immunosuppressive role of CTLA-4 to evade the immune system. By targeting checkpoint proteins such as CTLA-4 with antibodies, investigators can block the co-inhibitory activity of CTLA-4 and simulate T cell responses that attack tumors. By utilizing a high sensitivity ELISA kit, levels of CTLA-4 can be measured in both healthy and diseased state samples.
PD-L1
Enlisting a patient’s own immune system to fight cancer has been a longstanding dream for cancer biologists. Immune checkpoint inhibitors targeting molecules like programmed death-ligand 1 (PD-L1) help make the dream a reality and are now transforming today’s cancer therapy. PD-L1 therapy has shifted the approach to cancer treatment due to its durable effects, and its ability to target a broad range of cancers with manageable toxicity compared to traditional chemotherapy.2-4 Current diagnostic tests for PD-L1 use immunohistochemistry (IHC) to score the tumor microenvironment, but results can be inconsistent. With PD-L1 levels varying from different cancer types, an ELISA can provide quantitative results that are consistent, accurate and reliable from one experiment to the next.
B7-H1/PD-L1 protein expression and release in human cancer cells was investigated. PC-3 and LNCaP cells, were left untreated (Control), treated with LY294002, PMA, or pretreated with LY294002 and then PMA for 24 hours. PMA treatment increased membrane and soluble B7-H1/PD-L1 concentration in the more aggressive PC-3, but not LNCaP cells.
Additional Resources
References
- Wei, S.C. et al. (2018) Cancer Discov. 8:1069.
- Thompson, R.H. et al. (2005) Cancer 104:2084.
- Fife, B.T. and J.A. Bluestone (2008) Immunol. Rev 224:166.
- Spranger, S. et al. (2013) Sci Transl. Med 5:200ra116.