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Optimal Selection of IFN-α-Inducible Genes to Determine Type I Interferon Signature Improves the Diagnosis of Systemic Lupus Erythematosus

Journal

BIOMEDICINES
Volume 11, Issue 3, Pages -

Publisher

MDPI
DOI: 10.3390/biomedicines11030864

Keywords

IFN alpha; autoimmune disease; IFN-alpha-inducible genes; diagnostics; monitoring disease activity; autoantibodies; IFN-I; immunopathogenesis; inflammation; gene expression

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Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by the production of autoantibodies specific to self-molecules. Elevated type I interferon signature (IFN- I) in SLE leads to dysregulation of immune function and autoantibodies production. The most common method to determine IFN-I signature is measuring the gene expression of several IFN-a-inducible genes (IFIGs) in blood samples and calculating a score. The understanding of IFN-I signature in SLE can improve diagnosis and monitoring of disease activity.
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by the production of autoantibodies specific to self-molecules in the nucleus, cytoplasm, and cell surface. The diversity of serologic and clinical manifestations observed in SLE patients challenges the development of diagnostics and tools for monitoring disease activity. Elevated type I interferon signature (IFN- I) in SLE leads to dysregulation of innate and adaptive immune function, resulting in autoantibodies production. The most common method to determine IFN-I signature is measuring the gene expression of several IFN-a-inducible genes (IFIGs) in blood samples and calculating a score. Optimal selection of IFIGs improves the sensitivity, specificity, and accuracy of the diagnosis of SLE. We describe the mechanisms of the immunopathogenesis of IFN-I signature (IFNa production) and its clinical consequences in SLE. In addition, we explore the association between IFN-I signature, the presence of autoantibodies, disease activity, medical therapy, and ethnicity. We discuss the presence of IFN-I signature in some patients with other autoimmune diseases, including rheumatoid arthritis, systemic and multiple sclerosis, Sjogren's syndrome, and dermatomyositis. Prospective studies are required to assess the role of IFIG and the best combination of IFIGs to monitor SLE disease activity and drug treatments.

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