nCounter® Inflammation Panel

Helping Your Research

Studying the early inflammatory response is fundamental to understanding the immune response and treating disease. The nCounter® Inflammation Panel lets you perform multiplex gene expression analysis on human or mouse samples with more than 200 genes focused on the study of inflammation. These genes represent a broad range of relevant pathways related to inflammation that include apoptosis, EGF, interleukin signaling, Ras, T cell receptor, and Toll-like receptor signaling. Panel highlights include: 

  • Content useful for the study of asthma, allergy, arthritis, and neurological-related inflammation 
  • Coverage of anti-inflammatory drugs that modulate the inflammatory response 
  • Overlapping coverage between Human and Mouse panels for direct species comparison 
  • Customizable with up to 55 additional user-defined genes with the Panel Plus option

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Publications

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Single-cell and spatial multi-omics highlight effects of anti-integrin therapy across cellular compartments in ulcerative colitis

Ulcerative colitis (UC) is driven by immune and stromal subsets, culminating in epithelial injury. Vedolizumab (VDZ) is an anti-integrin antibody that is effective for treating UC.

In situ single-cell profiling sheds light on IFI27 localisation during SARS-CoV-2 infection

The utilization of single-cell resolved spatial transcriptomics to delineate immune responses during SARS-CoV-2 infection was able to identify M1 macrophages to have elevated expression of IFI27 in areas of infection.
The SARS-CoV-2 pandemic has affected over 600 million people to date, resulting in over 6.

Whole transcriptome profiling of placental pathobiology in SARS‐CoV‐2 pregnancies identifies placental dysfunction signatures

Objectives: Severe Acute Respiratory Syndrome Coronavirus 2 (SARS‐CoV‐2) virus infection in pregnancy is associated with higher incidence of placental dysfunction, referred to by a few studies as a ‘preeclampsia‐like syndrome’. However, the mechanisms underpinning SARS‐CoV‐2‐induced placental malfunction are still unclear.

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