Establishing Type I Interferon signatures to identify diseases and categorize pathology associated with interferon dysregulation
Presenter Status
Staff
Abstract Type
Translational Research
Primary Mentor or Principal Investigator
Todd Bradley
Presentation Type
Poster
Start Date
20-5-2026 11:00 AM
End Date
20-5-2026 12:00 PM
Abstract Text
Interferon (IFN) activation occurs during both viral and bacterial infections, traditionally as a mechanism of protection initiated by our immune systems and drives inflammation. However, increased interferon signaling has also been observed in several non-infectious disorders known as interferonopathies, such as system lupus erythematosus (SLE), Aicardi–Goutières syndrome (AGS), and proteasome-associated autoinflammatory syndromes (PRAAS/CANDLE). In some cases, IFN levels can predict disease onset and/or severity. Not only can genetic drivers like upregulation of interferon stimulating genes and activation of IFN associated pathways influence IFN production, anti-interferon antibodies produced by the host immune system can neutralize circulating interferon and mimic genetic reductions in interferon. Therapeutic strategies targeting IFN signaling, such as JAK inhibitors and anti-IFNα monoclonal antibodies, can improve outcomes for some patients suffering from these disorders. Here, we are establishing methodology for rapid identification of patient interferon signatures through both basal genetic or transcriptomic signatures and evaluation of blood-cell responsiveness to IFNα2a stimulation. These methods of analysis may provide the ability to quickly predict disease onset and severity and/or identify patients who would benefit from therapeutic interventions targeting the IFN pathway.
Establishing Type I Interferon signatures to identify diseases and categorize pathology associated with interferon dysregulation
Interferon (IFN) activation occurs during both viral and bacterial infections, traditionally as a mechanism of protection initiated by our immune systems and drives inflammation. However, increased interferon signaling has also been observed in several non-infectious disorders known as interferonopathies, such as system lupus erythematosus (SLE), Aicardi–Goutières syndrome (AGS), and proteasome-associated autoinflammatory syndromes (PRAAS/CANDLE). In some cases, IFN levels can predict disease onset and/or severity. Not only can genetic drivers like upregulation of interferon stimulating genes and activation of IFN associated pathways influence IFN production, anti-interferon antibodies produced by the host immune system can neutralize circulating interferon and mimic genetic reductions in interferon. Therapeutic strategies targeting IFN signaling, such as JAK inhibitors and anti-IFNα monoclonal antibodies, can improve outcomes for some patients suffering from these disorders. Here, we are establishing methodology for rapid identification of patient interferon signatures through both basal genetic or transcriptomic signatures and evaluation of blood-cell responsiveness to IFNα2a stimulation. These methods of analysis may provide the ability to quickly predict disease onset and severity and/or identify patients who would benefit from therapeutic interventions targeting the IFN pathway.
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Poster Board Number: 31