Researchers developed a quick and affordable whole-blood assay to detect autoantibodies against type I IFNs, enabling rapid diagnostics for immune disorders. This new method has potential clinical impact by addressing key limitations of current tests.
By Tarun Sai LomteReviewed by Susha Cheriyedath, M.Sc.Sep 25 2024 New whole-blood assay for detecting immune autoantibodies promises to revolutionize diagnostics, offering rapid, cost-effective solutions to detect inborn errors of immunity and neutralizing antibodies against type I interferons.
Autoantibodies against type I IFNs were first described in a patient with disseminated shingles in the early 1980s. They were long believed to be clinically silent, and their discovery in autoimmune polyendocrine syndrome type 1 patients led to their use as a diagnostic marker for APS-1. Currently, in vitro cell-based assays are available for detecting auto-Abs against type I IFNs.
Other tested molecules had poor induction. At the transcriptomic level, bulk RNA sequencing confirmed strong induction of CXCL10 expression in fresh peripheral blood mononuclear cells tested six hours after stimulation. Further, stimulation with IFN-β induced high IP-10, but stimulation with IFN-ω had a less pronounced induction of IP-10 relative to IFN-β or IFN-α2. Further, fresh PBMCs from three healthy donors were stimulated with IFN-α2, followed by bulk RNA sequencing .
Next, the researchers collected blood samples from five APS-1 patients and nine healthy individuals and stimulated them with IFN-α2, IFN-β, or IFN-ω. IP-10 levels were measured 16 hours after stimulation. The team observed robust induction of IP-10 in samples from healthy donors. Conversely, IP-10 induction was abolished in APS-1 patients after stimulation with IFN-ω or IFN-α2, revealing the neutralizing activity of auto-Abs in patients.
The previously observed neutralization data of these subjects were replicated using the whole-blood IP-10 assay. Finally, the researchers investigated the impact of genetic deficiency on type I IFN response. To this end, fresh blood from patients with complete IFN regulatory factor 9 , tyrosine kinase 2 , IFN-α/β receptor 1 , or IFNAR2 deficiency were stimulated.
Blood Allele Antibodies Assay Cell CXCL10 Diagnostic Diagnostics Genetic Immunity In Vitro Interferons Kinase Labor RNA RNA Sequencing Shingles Syndrome
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