PD-L1, FoxP3, CD8α Multiplex IHC Antibody Panel #78701

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).
FoxP3 is a transcription factor that is crucial for the development of T cells with regulatory properties (Treg) (13). Mutations in FoxP3 are associated with immune dysregulation, polyendocrinopathy, enteropathy, and X-linked syndrome (IPEX) (15), while overexpression in mice causes severe immunodeficiency (15). Research studies have shown that FoxP3 functions as a tumor suppressor in several types of cancer (16-18).
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 (19).