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IL28B, IL29 and micro-RNA 548 in subacute sclerosing panencephalitis as a rare disease

Gunes Cakmak Genc1, Ahmet Dursun1, Sevim Karakas Celik2

  • 1Faculty of Medicine, Department of Medical Genetics, Bulent Ecevit University, Zonguldak, Turkey.

Gene
|August 6, 2018
PubMed

Insights

Subacute sclerosing panencephalitis (SSPE) involves higher levels of interleukin-29 (IL-29) and specific microRNAs (miRNAs) in patients, suggesting an overactive immune response. Gene variations like rs8099917 also increase SSPE risk.

Area of Science:

  • Immunology
  • Neuroscience
  • Virology

Background:

  • Subacute sclerosing panencephalitis (SSPE) is a fatal neurodegenerative disease caused by persistent measles virus infection.
  • Interferon-lambdas (IFN-λs), including IL-28B and IL-29, are crucial cytokines in antiviral responses.
  • Elevated IL-29 levels and altered immune responses are implicated in SSPE pathogenesis.

Purpose of the Study:

  • To investigate the contribution of IL-28B, IL-29 levels, and gene polymorphisms to immune dysfunction in SSPE.
  • To explore the association between the miR-548 family, IL-29, and SSPE development.
  • To identify potential biomarkers for SSPE risk and progression.

Main Methods:

  • Genotyping for IL28B polymorphisms (rs12979860, rs8099917, rs30461) in 64 SSPE patients and 68 controls.
  • Quantification of serum IL-28B and IL-29 levels.
  • Measurement of miR-548b, miR-548c, and miR-548i expression levels in patients and controls.

Main Results:

  • SSPE patients exhibited significantly higher serum IL-29 levels compared to healthy controls.
  • The G allele of the rs8099917 polymorphism was significantly more frequent in SSPE patients, increasing SSPE risk 2.183-fold.
  • Expression levels of miR-548b-5p, miR-548c-5p, and miR-548i were significantly elevated in SSPE patients.

Conclusions:

  • Elevated IL-29 and miR-548 expression in SSPE patients may represent a compensatory immune response.
  • Specific IL28B gene polymorphisms, particularly rs8099917, are associated with increased SSPE risk.
  • These findings highlight the role of specific cytokines and miRNAs in SSPE pathogenesis and suggest potential therapeutic targets.

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