nCounter® Immune Exhaustion Panel
Helping Your Research
Uncover the mechanisms behind T cell, B cell, and NK cell exhaustion in diverse contexts, including cancer and infectious disease, with a 785 gene panel that gets you results in less than 24 hours and is compatible with a broad range of sample types. Characterize immune status, develop signatures for assessing the exhausted state, and identify novel therapeutic targets to prevent or reverse exhaustion.
How It Works
- Directly profile 785 genes across 47 pathways involved in immune exhaustion:
- Immune Activation
- Immune Suppression
- Immune Status
- Immune Checkpoints
- Metabolism & Microenvironment
- Understand the mechanisms of exhaustion in T cells, B cells, NK cells, CAR-T cells and other adoptive immune cells
- Discover novel therapeutic targets for preventing or reversing immune exhaustion
- Determine the extent of a peripherally suppressed, adaptive immune response to cancer with the 18-gene Tumor Inflammation Signature (TIS)
- Quantify the presence and relative abundance of 14 different immune cell types
Chronic infections caused by viruses and other pathogens can induce immune exhaustion. The Human Immune Exhaustion Panel includes probes for Epstein-Barr virus (EBV) and Cytomegalovirus (CMV), and the Mouse Immune Exhaustion Panel includes probes for Lymphocytic Choriomeningitis (LCMV). The panel can be supplemented with up to 55 genes of your choice with a Panel Plus spike-in for studying exhaustion in the context of different types of infectious disease.
The 18-gene Tumor Inflammation Signature (TIS) is included in the panel gene list and measures activity known to be associated with PD-1/PD-L1 inhibitors. Customers have the option to purchase a standalone TIS report with the Immune Exhaustion Panel.
- Includes four axes of biology that characterize a peripherally suppressed, adaptive immune response, including:
- Antigen presenting cells
- T cell/NK cell presence
- IFNγ biology
- T cell exhaustion
- Tissue-of-origin agnostic (Pan-Cancer)
- Potential surrogate for PD-L1 and mutational load in a research setting
Combined MEK and JAK/STAT3 pathway inhibition effectively decreases SHH medulloblastoma tumor progression.
Medulloblastoma (MB) is the most common primary malignant pediatric brain cancer. We recently identified novel roles for the MEK/MAPK pathway in regulating human Sonic Hedgehog (SHH) MB tumorigenesis.
Immune suppression in the tumor-draining lymph node corresponds with distant disease recurrence in patients with melanoma.
Immune checkpoint blockade (ICB) using anti-PD-1/PD-L1 and anti-CTLA-4 antibodies significantly enhances survival in metastatic melanoma patients and has recently been shown to prolong relapse-free survival in stage III and high-risk stage II melanoma patients ( Eggermont et al. , 2018; Luke et al.
Multidimensional Immunophenotyping of Intraductal Papillary Mucinous Neoplasms Reveals Novel T Cell and Macrophage Signature.
Background: Intraductal papillary mucinous neoplasms (IPMN) are the only radiographically identifiable precursor to pancreatic adenocarcinoma, yet little is known about how these lesions progress to cancer. Inflammation has been associated with dysplastic progression; however, the cause and composition of this inflammation remains poorly characterized.
The nCounter Immune Exhaustion Panel enables researchers to explore the mechanisms behind T cell, B cell, and NK cell exhaustion in diverse contexts, including cancer and infectious disease.
The Immune Exhaustion Panel provides comprehensive coverage of the most relevant immune checkpoints that can potentially be used to modulate the dynamics of the immune response.