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Ring Finger Protein 215 Negatively Regulates Type I IFN Production via Blocking NF-κB p65 Activation

Yun Wu1,2, Delin Chen1,3, Yiwen Hu4

  • 1Key Laboratory of Tropical Disease Control, Ministry of Education, Sun Yat-sen University, Guangzhou, China.

Journal of Immunology (Baltimore, Md. : 1950)
|November 25, 2022
PubMed

Insights

Ring finger protein 215 (RNF215) inhibits type I interferon production during viral infections. This protein may be a therapeutic target for autoimmune diseases linked to abnormal interferon activity.

Area of Science:

  • Immunology
  • Molecular Biology
  • Virology

Background:

  • Pattern recognition receptors (PRRs) detect pathogen-associated molecular patterns (PAMPs) during viral infections, inducing interferons (IFNs) and an antiviral state.
  • Dysregulated IFN signaling can lead to immunopathology and autoimmune diseases like systemic lupus erythematosus (SLE).
  • Precise regulation of IFN signaling is crucial for immune homeostasis, but regulatory mechanisms are not fully understood.

Purpose of the Study:

  • To identify novel regulators of type I interferon production.
  • To investigate the role of ring finger protein 215 (RNF215) in viral infection and IFN signaling.
  • To explore the potential involvement of RNF215 in autoimmune diseases.

Main Methods:

  • Investigated RNF215 expression in human macrophages upon viral infection.
  • Examined RNF215 interaction with NF-κB subunits (p65).
  • Assessed RNF215's effect on IFNB1 promoter activity and NF-κB binding.
  • Correlated RNF215 expression with type I IFN levels in SLE patients.

Main Results:

  • RNF215 expression was upregulated by viral infection in human macrophages.
  • RNF215 was found to inhibit type I IFN production by interacting with p65 and repressing NF-κB binding to the IFNB1 promoter.
  • RNF215 expression negatively correlated with type I IFNs in patients with systemic lupus erythematosus.

Conclusions:

  • RNF215 acts as a negative regulator of type I interferon production.
  • RNF215 plays a role in the pathogenesis of autoimmune diseases characterized by aberrant IFN production.
  • RNF215 represents a potential therapeutic target for diseases involving excessive IFN signaling.

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