A defect in COPI-mediated transport of STING causes immune dysregulation in COPA syndrome.


Journal

The Journal of experimental medicine
ISSN: 1540-9538
Titre abrégé: J Exp Med
Pays: United States
ID NLM: 2985109R

Informations de publication

Date de publication:
02 11 2020
Historique:
received: 21 05 2020
revised: 07 07 2020
accepted: 08 07 2020
entrez: 30 7 2020
pubmed: 30 7 2020
medline: 11 3 2021
Statut: ppublish

Résumé

Pathogenic COPA variants cause a Mendelian syndrome of immune dysregulation with elevated type I interferon signaling. COPA is a subunit of coat protein complex I (COPI) that mediates Golgi to ER transport. Missense mutations of the COPA WD40 domain impair binding and sorting of proteins targeted for ER retrieval, but how this causes disease remains unknown. Given the importance of COPA in Golgi-ER transport, we speculated that type I interferon signaling in COPA syndrome involves missorting of STING. We show that a defect in COPI transport causes ligand-independent activation of STING. Furthermore, SURF4 is an adapter molecule that facilitates COPA-mediated retrieval of STING at the Golgi. Activated STING stimulates type I interferon-driven inflammation in CopaE241K/+ mice that is rescued in STING-deficient animals. Our results demonstrate that COPA maintains immune homeostasis by regulating STING transport at the Golgi. In addition, activated STING contributes to immune dysregulation in COPA syndrome and may be a new molecular target in treating the disease.

Identifiants

pubmed: 32725126
pii: 151981
doi: 10.1084/jem.20201045
pmc: PMC7596814
pii:
doi:

Substances chimiques

Coatomer Protein 0
Interferon Type I 0
Membrane Proteins 0
STING1 protein, human 0
SURF4 protein, human 0
Sting1 protein, mouse 0
Surf4 protein, mouse 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : NHLBI NIH HHS
ID : P01 HL103453
Pays : United States
Organisme : NHLBI NIH HHS
ID : R00 HL135403
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI137249
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL122533
Pays : United States

Commentaires et corrections

Type : CommentIn

Informations de copyright

© 2020 Deng et al.

Déclaration de conflit d'intérêts

Disclosures: T. Martinu reported grants from Sanofi and non-financial support from APCBio outside the submitted work. No other disclosures were reported.

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Auteurs

Zimu Deng (Z)

Department of Medicine, University of California, San Francisco, San Francisco, CA.

Zhenlu Chong (Z)

Department of Medicine, University of California, San Francisco, San Francisco, CA.

Christopher S Law (CS)

Department of Medicine, University of California, San Francisco, San Francisco, CA.

Kojiro Mukai (K)

Laboratory of Organelle Pathophysiology, Department of Integrative Life Sciences, Graduate School of Life Sciences, Tohoku University, Sendai, Japan.

Frances O Ho (FO)

Department of Medicine, University of California, San Francisco, San Francisco, CA.

Tereza Martinu (T)

Toronto Lung Transplant Program, University Health Network, University of Toronto, Toronto, Ontario, Canada.

Bradley J Backes (BJ)

Department of Medicine, University of California, San Francisco, San Francisco, CA.

Walter L Eckalbar (WL)

Department of Medicine, University of California, San Francisco, San Francisco, CA.

Tomohiko Taguchi (T)

Laboratory of Organelle Pathophysiology, Department of Integrative Life Sciences, Graduate School of Life Sciences, Tohoku University, Sendai, Japan.

Anthony K Shum (AK)

Department of Medicine, University of California, San Francisco, San Francisco, CA.
Cardiovascular Research Institute, University of California, San Francisco, San Francisco, CA.

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Classifications MeSH