The immune system employs a series of checkpoints to protect normal, healthy tissue from an immune response. These consist of receptors on the surface of activated T cells and their corresponding ligands on the surface of antigen presenting cells. A key immune checkpoint is triggered when PD-1 (programmed cell death protein 1) engages its ligand PD-L1. As a result of this interaction, T cell activation is attenuated and an active immune response is prevented(1).
This mechanism is often co-opted by tumors. PD-L1 is upregulated in several tumor types and contributes to the malignancy of these cancers by interacting with PD-1 and inhibiting T cell activation. In this way, the tumors avoid detection and destruction by the immune system(1-3). Accordingly, PD-1 and PD-L1 have garnered much attention for their roles in tumor immunology and as immune-based therapeutic targets(4,5).
|Product Name||PD-L1 (E1L3N®) XP® Rabbit mAb #13684||PD-L1 (405.9A11) Mouse mAb #29122||PD-L1 (Extracellular Domain Specific) (E1J2J) Rabbit mAb #15165|
|Antibody host species||Rabbit||Mouse||Rabbit|
|IHC analysis of paraffin-embedded human placenta|
|Recommended usage for IHC||Preferred clone based on sensitivity||Use when multiplexing with rabbit antibodies||Use for studying the extracellular domain of PD-L1|
Western blot analysis of lysates from:
Flow cytometric analysis of untreated SUP-M2 cells using PDL1 (E1L3N®) XP® Rabbit mAb #13864 (blue) compared to concentration matched Rabbit (DA1E) mAb IgG XP® Isotype Control #3900 (red). Anti-rabbit IgG (H+L), F(ab')2 Fragment (Alexa Fluor® 647 Conjugate) #4414 was used as a secondary antibody.