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
Sympathetic axonal sprouting induces changes in macrophage populations and protects against pancreatic cancer.
Neuronal nerve processes in the tumor microenvironment were highlighted recently. However, the origin of intra-tumoral nerves remains poorly known, in part because of technical difficulties in tracing nerve fibers via conventional histological preparations.
Immunostimulatory cancer-associated fibroblast subpopulations can predict immunotherapy response in head and neck cancer.
Purpose: Cancer-associated fibroblasts (CAF) have been implicated as potential mediators of checkpoint immunotherapy response. However, the extensive heterogeneity of these cells has precluded rigorous understanding of their immunoregulatory role in the tumor microenvironment.
Spatial profiling reveals association between WNT pathway activation and T-cell exclusion in acquired resistance of synovial sarcoma to NY-ESO-1 transgenic T-cell therapy.
Background: Genetically engineered T-cell immunotherapies for adoptive cell transfer (ACT) have emerged as a promising form of cancer treatment, but many of these patients develop recurrent disease. Furthermore, delineating mechanisms of resistance may be challenging since the analysis of bulk tumor profiling can be complicated by spatial heterogeneity.
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.