PD-L1, CD3ε, CD8α Multiplex IHC Antibody Panel #65713

The field of cancer immunotherapy is focused on empowering the immune system to fight cancer. This approach has seen recent success in the clinic with targeting immune checkpoint control proteins, such as PD-1 (1,2). Despite this success, clinical biomarkers that predict response to therapeutic strategies involving PD-1 receptor blockade are still under investigation (3-5). While PD-L1 expression has been linked with an increased likelihood of response to anti-PD-1 therapy, research studies have shown that additional factors, such as tumor-immune infiltration and the ratio of effector to regulatory T cells within the tumor, could play a significant role in predicting treatment outcome (6-9).
Programmed cell death 1 ligand 1 (PD-L1) is a member of the B7 family of cell surface ligands that regulate T cell activation and immune responses. The PD-L1 ligand binds the PD-1 transmembrane receptor and inhibits T cell activation. PD-L1 is expressed in several tumor types, including melanoma, ovary, colon, lung, breast, and renal cell carcinomas (10-12).
CD3 (Cluster of Differentiation 3) is a multiunit protein complex that directly associates with the T cell receptor (TCR). CD3 is composed of four polypeptides (ζ, γ, ε and δ), each of which contains at least one immunoreceptor tyrosine-based activation motif (ITAM) (13). Engagement of TCR complex with foreign antigens induces tyrosine phosphorylation in the ITAM motifs and phosphorylated ITAMs function as docking sites for signaling molecules such as ZAP-70 and p85 subunit of PI-3 kinase (14,15).
CD8 (Cluster of Differentiation 8) is a disulphide-linked heterodimer consisting of α and β subunits. On T cells, CD8 is the coreceptor for the TCR, and these two distinct structures recognize the Antigen–Major Histocompatibility Complex (MHC). CD8 ensures specificity of the TCR–antigen interaction, prolongs the contact between the T cell and the antigen presenting cell, and the α chain recruits the tyrosine kinase Lck, which is essential for T cell activation (16).