nCounter® Autoimmune Profiling Panel
Helping Your Research
Get insights into immune system dysfunction quickly with our comprehensive 770 gene multiplex panel for human or mouse to evaluate the pathways, processes, and cell types involved in autoimmune disease, chronic inflammatory disease, and immunotherapy-related adverse events. Analyze autoimmune biomarkers rapidly without the need for qPCR or NGS.
- Therapeutic mechanism of action (MOA) studies
- Immunotherapy-induced adverse event investigations
- Discovery/validation of disease and therapeutic specific biomarkers
- Development of predictive signatures of drug response
- Compatible with challenging sample types such as PBMCs and FFPE
How it Works
The nCounter Autoimmune Profiling panels are designed to rapidly characterize the biology behind autoimmune disease and an aberrant immune response. Each human and mouse panel allow for a comprehensive evaluation of pathways, processes, and cell types that are involved in autoimmune disease and chronic inflammatory disorders.
Comprehensive assessment of 35 pathways and processes associated with autoimmune disease and chronic inflammatory disorders
Unique cell typing analysis feature measures the relative abundance of 14 different immune cell types
Customizable with Panel Plus option – add up to 55 genes of your choice
Streamlined workflow with just 15 minutes total hands-on time
Panel Selection Tool
Find the gene expression panel for your research with easy to use panel proFind Your Panel
The TruCulture-NanoString Solution for Immune Profiling
Recent publications (1,2) from the Milieu Interieur project at Institut Pasteur have shown the utility of the Myriad RBM TruCulture(1) whole blood collection and culture system paired with nCounter gene expression analysis.
For more information on the combined TruCulture-NanoString workflow, visit the Myriad TruCulture site.
In the Lab
The 35 pathways and processes in this panel provide a comprehensive view into immune system dysfunction in autoimmune disease and treatment-induced adverse immune events.
The Autoimmune Profiling Panels include unique cell profiling signatures to measure the relative abundance of 14 different immune cell types1. The table below summarizes each cell type represented by gene content in the panel, as qualified through biostatistical approaches and selected literature in the field of immunology.
The Autoimmune Profiling Panel is designed to encompass adaptive and innate immune system dysfunction associated with six of the most common and debilitating autoimmune diseases. The table below describes the six conditions that were emphasized in creating this panel, along with induced adverse immune events associated with immunotherapy. While this panel was designed around these six diseases, it will provide powerful immune system information for the research of any autoimmune or chronic inflammatory disorder.
Content in the Autoimmune Profiling Panel includes targets for more than 30 approved and investigational therapies for autoimmune disease and chronic inflammatory disorders.
Diabetes induces dysregulation of microRNAs associated with survival, proliferation and self-renewal in cardiac progenitor cells.
AIMS/HYPOTHESIS: Diabetes mellitus causes a progressive loss of functional efficacy in stem cells, including cardiac progenitor cells (CPCs). The underlying molecular mechanism is still not known.
Rapid Induction of Pulmonary Inflammation, Autoimmune Gene Expression, and Ectopic Lymphoid Neogenesis Following Acute Silica Exposure in Lupus-Prone Mice.
Occupational exposure to crystalline silica (cSiO2) is etiologically associated with systemic lupus erythematosus (lupus) and other autoimmune diseases. cSiO2’s autoimmune effects in humans can be mimicked chronically in female lupus-prone NZBWF1 mice following repeated exposure to the particle.
A Novel Inflammatory Dendritic Cell That Is Abundant and Contiguous to T Cells in the Kidneys of Patients With Lupus Nephritis.
The mechanisms that promote local inflammatory injury during lupus nephritis (LN) flare are largely unknown. Understanding the key immune cells that drive intrarenal inflammation will advance our knowledge of disease pathogenesis and inform the development of new therapeutics for LN management.