AI Article Synopsis

  • Systemic lupus erythematosus (SLE) is an autoimmune disease that triggers inflammation in various organs due to immune complex buildup and is influenced by type I interferons (IFNs) that indicate disease activity.* -
  • Genetic and environmental factors lead to abnormal activation of the immune system, and IFNs play a key role in the disease's development through the Janus kinase-signal transducer and activator of transcription pathway.* -
  • Anifrolumab (Saphnelo) is an FDA-approved monoclonal antibody treatment for moderate to severe SLE, given as an intravenous infusion every four weeks, targeting type I interferon receptors to help regulate inflammation.*

Article Abstract

Systemic lupus erythematosus (SLE) is an autoimmune disease which causes damaging inflammation in multiple organs via the accumulation of immune complexes. SLE pathogenesis is associated with type I interferons (IFNs), which are central and reflective of disease activity in SLE. Even before clinical development of disease, genetic and environmental contributions to IFN production lead to abnormal innate and adaptive immune activation. Through the Janus kinase-signal transducer and activator of transcription signaling pathway, IFN play a central role in the immunopathogenicity of SLE. Thus, IFN-blocking therapy may be used to regulate inflammation in individuals with SLE. Food and Drug Administration (FDA)-approved anifrolumab (Saphnelo), which is a human IgG1κ monoclonal antibody that binds to subunit 1 of the type I interferon receptor with high specificity and affinity, was also approved for the treatment of adult patients with moderate to severe SLE who are receiving standard therapy by Pharmaceuticals and Medical Device Agency (PMDA), in Japan in September 2021; anifrolumab is administered as an intravenous infusion, 300 mg over a 30-minute period, every 4 weeks. In this article, we reviewed the actions of type I IFN and anifrolumab as a treatment for SLE.

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Source
http://dx.doi.org/10.1254/fpj.22026DOI Listing

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