Dysregulation of antiviral helicase pathways in systemic lupus erythematosus

Luciana Oliveira, Nailú A. Sinicato, Mariana Postal, Simone Appenzeller, Timothy B. Niewold

Research output: Contribution to journalArticle

9 Scopus citations

Abstract

In the autoimmune disease systemic lupus erythematosus (SLE), our normal antiviral defenses are inappropriately activated, resulting in over-activity of the type I interferon (IFN) pathway. This increased activity of the type I IFN pathway is an important primsary pathogenic factor in the disease. Emerging evidence has implicated the antiviral helicases in this process. The antiviral helicases normally function as nucleic acid receptors in viral immunity. Genetic variations in antiviral helicase genes have been associated with SLE, supporting the idea that helicase pathways are involved in the primary pathogenesis of SLE. Studies have documented functional consequences of these genetic variations within the type I IFN pathway in human cell lines and SLE patients. In this review, we summarize the function of helicases in the anti-viral immune response, and how this response is dysregulated in SLE patients. In particular, we will focus on known functional genetic polymorphisms in the IFIH1 (MDA5) and mitochondrial antiviral signaling protein genes which have been implicated in human SLE. These data provide fascinating evidence for dysregulation of helicase-mediated innate immunity in SLE, and may support novel therapeutic strategies in the disease.

Original languageEnglish (US)
Article number418
JournalFrontiers in Genetics
Volume5
Issue numberNOV
DOIs
StatePublished - 2014

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Keywords

  • Antiviral helicase
  • Interferon
  • Systemic lupus erythematosus

ASJC Scopus subject areas

  • Genetics
  • Molecular Medicine
  • Genetics(clinical)

Cite this

Oliveira, L., Sinicato, N. A., Postal, M., Appenzeller, S., & Niewold, T. B. (2014). Dysregulation of antiviral helicase pathways in systemic lupus erythematosus. Frontiers in Genetics, 5(NOV), [418]. https://doi.org/10.3389/fgene.2014.00418