nCounter® Host Response Panel
Helping Your Research
Understanding the complex interplay between a pathogen and the host response is important to developing effective vaccines and therapeutics to fight infectious disease. The nCounter® Host Response Panel helps researchers study the phases and progression of infection across the major components of the human or mouse host response with pathogen-agnostic content optimized for blood but suitable for all sample types. The panel was specifically developed for understanding the complexities of the immune response to infectious disease, including COVID-19.
How it Works
The Host Response Panel helps rapidly advance knowledge of emerging infectious disease with experiments that take minutes to set-up and get you results in less than 24 hours.
- Study the five elements of the host response in human or mouse samples
- Host Susceptibility
- Interferon Response
- Innate Immune Cell Activation
- Adaptive Immune Response
- Profile 785 genes in human or mouse genes across 50+ pathways
- Detect the presence of a pathogen and evaluate organ-specific tissue damage with a Panel Plus spike-in of up to 55 genes
- Develop signatures of host response dynamics
- Identify and validate biomarkers for disease severity
- Evaluate the effect of vaccines & therapies
Customize your research project by adding tissue or pathogen-specific probes to the Host Response Panel with a 55-gene Panel Plus. Add the off-the-shelf 20-gene Coronavirus Panel Plus to study SARS-CoV-2 and other coronaviruses or build your own Panel Plus gene list with transcripts specific for different tissue types. Mix and match transcripts from the pathogen of your choice and additional host tissue markers to add a Panel Plus to the Host Response Panel for studying the pathogenesis of various infectious diseases. Check out the Human or Mouse Host Response Tissue Gene Lists to see which genes to add as a Panel Plus spike-in to study the effect of infectious disease on different organs.
Panel Selection Tool
Find the gene expression panel for your research with easy to use panel proFind Your Panel
Take advantage of comprehensive coverage of the most relevant immune checkpoints to study modulation of the host immune response and subsequent inflammatory cascade.
Probes included in the Human Host Response Panel have high homology to non-human primates (NHPs), allowing for seamless comparative infectious disease research as well as preclinical studies. Percent identity is used to estimate likelihood of the probe functioning on non-human primate targets. Additional comparisons with other NHP species are available upon request.
Genes included in the Host Response Panel provide unique cell profiling data to measure the relative abundance of 14 different immune cell types. The table below summarizes the genes included in each cell type signature, as qualified through biostatistical approaches and selected literature in the field
EGR1 as a potential marker of prognosis in extranodal NK/T-cell lymphoma.
Extranodal natural killer T-cell lymphoma (ENKTL) is an aggressive malignancy with a dismal prognosis. In the present study, gene expression profiling was performed to provide more information on ENKTL molecular signature and offer a rationale for further investigation of prognostic markers in ENKTL.
Acute inflammatory profiles differ with sex and age after spinal cord injury.
BACKGROUND: Sex and age are emerging as influential variables that affect spinal cord injury (SCI) recovery. Despite a changing demographic towards older age at the time of SCI, the effects of sex or age on inflammation remain to be elucidated.
The clinical significance of receiving a kidney allograft from deceased donor with chronic histologic changes.
Allograft survival of deceased donor kidneys with suboptimal histology (DRTx/suboptimal histology: >10% glomerulosclerosis, >10% tubulointerstitial scarring, or >mild vascular sclerosis) is inferior to both DRTx with optimal histology (DRTx/optimal histology) and living donor kidneys irrespective of histologic changes (LRTx). In this report, we explored the reasons behind this guarded outcome with a special focus on the role of alloimmunity.