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Epistaxis, or nosebleeds, occurs when small, swollen blood vessels in the nasal mucous membrane rupture. Typically, the anterior septum is the primary site of occurrence.
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Related Experiment Video

Updated: Dec 7, 2025

RNAi-mediated Double Gene Knockdown and Gustatory Perception Measurement in Honey Bees Apis mellifera
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COPA silences STING.

Sophie Rivara1, Andrea Ablasser1

  • 1Global Health Institute, Swiss Federal Institute of Technology Lausanne, Lausanne, Switzerland.

The Journal of Experimental Medicine
|September 29, 2020
PubMed
Summary

Mutations in COPA cause}

Area of Science:

  • Immunology
  • Molecular Biology
  • Genetics

Background:

  • COPA syndrome is an autoimmune disorder characterized by high interferon titers.
  • The precise molecular mechanisms underlying COPA syndrome pathogenesis remain incompletely understood.

Purpose of the Study:

  • To investigate the link between COPA syndrome and interferon dysregulation.
  • To elucidate the molecular mechanisms by which COPA mutations lead to chronic immune activation.

Main Methods:

  • Analysis of patient samples with COPA syndrome.
  • Investigating the role of COPA mutations in the STING pathway.
  • Studying protein trafficking between the ER and Golgi apparatus.

Main Results:

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  • Mutations in COPA prevent the retrieval of STING (stimulator of interferon genes) from the Golgi apparatus back to the endoplasmic reticulum (ER).
  • This impaired STING trafficking leads to chronic immune activation and high interferon titers.
  • Four independent studies corroborate these findings.

    • Conclusions:

    • COPA syndrome pathogenesis involves a defect in COPA protein function, disrupting STING localization.
    • This disruption results in constitutive type I interferon production, driving autoimmune manifestations.
    • Targeting the STING pathway may offer therapeutic strategies for COPA syndrome.