Immune Response

Comprehensive Characterization of Immune Response to Disease

Immune system dysfunction is associated with over 80 autoimmune disorders. Autoimmune disorders, such as type 1 diabetes, rheumatoid arthritis, systemic lupus erythematosus (SLE) and inflammatory bowel disease (IBD) are characterized by dysregulated responses mediated primarily by inflammatory cytokines and auto-antibodies. The HTG EdgeSeq Immune Response Panel measures 2,002 mRNAs associated with the body’s immune response throughout disease progression, including response to autoimmune disease and pathogens such as SARS-CoV-2.

Measure Genes Associated with Disease Progression of Innate Immune Response

Map New Biomarkers Using Expression of Autoimmune Disease

Identify Innate Pathogen Response and Pathway Identification

Characterize COVID-19 Disease Progression and Severity Through Gene Expression

Measure Disease Progression with Innate Immune Response

The HTG EdgeSeq Immune Response Panel can characterize the body’s transcriptional response through the five major phases of pathogen infection: incubation, prodromal, illness, decline and convalescence periods.

Map New Biomarkers Using Expression of Autoimmune Disease

Targeted gene expression profiling is a powerful tool that can be used to identify autoimmune disease markers as well as the host immune response. Comparison of gene expression to normal samples can then be used to identify gene networks involved in disease progression.

Innate Pathogen Response and Pathway Identification

How cells respond to pathogen-mediated disruption of gene expression to initiate protective responses remains largely unclear. Targeting specific portions of the transcriptome involved in response can help researchers answer questions related to the pathogen-mediated disruption of gene expression as well as identify biomarkers involved in the innate immune response.

Characterize COVID-19 Disease Progression and Severity Through Gene Expression

Blanco-Melo et al. were the first peer reviewed publication to show that the transcription footprint of SARS-CoV-2 infection is distinct in comparison to the other viruses, including Respiratory Syncytial Virus (RSV), Human Parainfluenza Virus (HPIV) and Influenza A. While they noted that SARS-CoV-2 infection showed a robust chemokine signature, it failed to launch a robust IFN-I/-III response. These findings highlight the fundamental importance of gene expression profiling on understanding COVID-19 disease progression and severity.