Evidence map›Paper›PMID 40111902›Full record

ArticleeLife2025

Tissue inflammation induced by constitutively active STING is mediated by enhanced TNF signaling.

Hella Luksch, Felix Schulze, David Geißler-Lösch, David Sprott, Lennart Höfs, Eva M Szegö, Wulf Tonnus, Stefan Winkler, Claudia Günther, Andreas Linkermann and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in eLife, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

  1. Review
  2. Autoinflammatory syndromes of STING and TREX1 dysfunction.The Journal of clinical investigation · 2026
    Review
  3. A STING for necroptosis.Cell death and differentiation · 2026
    Article
  4. Review
  5. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Hella LukschDepartment of Pediatrics, Faculty of Medicine and University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.ORCID https://orcid.org/0000-0001-7070-4992
Felix SchulzeDepartment of Pediatrics, Faculty of Medicine and University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.ORCID https://orcid.org/0000-0002-8220-5012
David Geißler-LöschDepartment of Neurology, Faculty of Medicine and University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.ORCID https://orcid.org/0009-0006-8332-2145
David SprottDepartment of Physiology, Faculty of Medicine and University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
Lennart HöfsDepartment of Neurology, Faculty of Medicine and University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
Eva M SzegöDepartment of Neurology, Faculty of Medicine and University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
Wulf TonnusDivision of Nephrology, Department of Internal Medicine III, Faculty of Medicine and University Hospital Carl Gustav, Dresden, Germany.ORCID https://orcid.org/0000-0002-9728-1413
Stefan WinklerDepartment of Pediatrics, Faculty of Medicine and University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
Claudia GüntherDepartment of Dermatology, Faculty of Medicine and University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.ORCID https://orcid.org/0000-0002-4330-1861
Andreas LinkermannDivision of Nephrology, Department of Internal Medicine III, Faculty of Medicine and University Hospital Carl Gustav, Dresden, Germany.ORCID https://orcid.org/0000-0001-6287-9725
Rayk BehrendtInstitute for Clinical Chemistry and Clinical Pharmacology, University Hospital Bonn, Bonn, Germany.ORCID https://orcid.org/0000-0002-1091-2877
Lino L TeichmannDepartment of Medicine III, University Hospital Bonn, Bonn, Germany.ORCID https://orcid.org/0000-0001-9489-7282
Björn H FalkenburgerDepartment of Neurology, Faculty of Medicine and University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.ORCID https://orcid.org/0000-0002-2387-526X
Angela Rösen-WolffDepartment of Pediatrics, Faculty of Medicine and University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.ORCID https://orcid.org/0000-0002-9613-5879

Funding

Deutsche Forschungsgemeinschaft 369799452-TRR237Deutsche Forschungsgemeinschaft EXC2151 - 390873048
6 · The paper itself

Abstract

Constitutive activation of STING by gain-of-function mutations triggers manifestation of the systemic autoinflammatory disease STING-associated vasculopathy with onset in infancy (SAVI). In order to investigate the role of signaling by tumor necrosis factor (TNF) in SAVI, we used genetic inactivation of TNF receptors 1 and 2 in murine SAVI, which is characterized by T cell lymphopenia, inflammatory lung disease, and neurodegeneration. Genetic inactivation of TNFR1 and TNFR2, however, rescued the loss of thymocytes, reduced interstitial lung disease, and neurodegeneration. Furthermore, genetic inactivation of TNFR1 and TNFR2 blunted transcription of cytokines, chemokines, and adhesions proteins, which result from chronic STING activation in SAVI mice. In addition, increased transendothelial migration of neutrophils was ameliorated. Taken together, our results demonstrate a pivotal role of TNFR signaling in the pathogenesis of SAVI in mice and suggest that available TNFR antagonists could ameliorate SAVI in patients.

Indexed as

InflammationMembrane ProteinsSignal TransductionTumor Necrosis Factor-alphaAnimalsMiceMice, Inbred C57BLReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IISTING ProteinMembrane ProteinsReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IISting1 protein, mouseSTING ProteinTnfrsf1a protein, mouseTnfrsf1b protein, mouseTumor Necrosis Factor-alphaimmunologyinflammationmouseSAVISTINGsystemic autoinflammationTNFvasculopathy

Identifiers

PMID40111902
PMCPMC11996172

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.