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Area of Science:

  • Immunology
  • Molecular Biology
  • Genetics

Background:

  • Type I interferons (IFNαβ) orchestrate a broad gene expression program crucial for immunity.
  • Dysregulation of IFNαβ signaling can lead to pathogenic immune responses and autoinflammatory diseases called interferonopathies.

Purpose of the Study:

  • This review focuses on the molecular mechanisms underlying pathogenic Type I interferon signaling.
  • It highlights recent advances in understanding mutations affecting nucleic acid recognition, negative feedback, and proteasome function.

Main Methods:

  • The review synthesizes recent findings on cytoplasmic DNA and RNA sensing pathways.
  • It discusses genetic mutations impacting these pathways and their link to interferonopathies.

Main Results:

  • Recent advances clarify how self-DNA is sensed by cGAS and self-RNA by RIG-I/MDA-5.
  • Mutations in DNase-II, ADAR1, Pol α, RIG-I, and MDA-5 are linked to aberrant IFNαβ induction.
  • Novel molecular interactions in monogenic autoinflammatory diseases are being defined.

Conclusions:

  • Understanding the precise mechanisms of IFNαβ regulation is key to deciphering interferonopathies.
  • Genetic defects in nucleic acid metabolism and immune sensing pathways are significant contributors to these diseases.