Evidence map›Paper›PMID 41807847›Full record

ArticleNature neuroscience2026

Persistent interferon signaling causes sensory neuron plasticity and pain before and during arthritis.

Jie Su, Ming-Dong Zhang, Jussi Kupari, Dongoh Kwak, Laurence Picton, Bingze Xu, Leandro Flores do Nascimento, Yizhou Hu, Alejandro Gonzalez, Dmitry Usoskin and 5 more

Abstract read
In one paragraph

Article in Nature neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

15 authors.

Jie SuDepartment of Medical Biochemistry and Biophysics, Division of Molecular Neurobiology, Karolinska Institutet, Stockholm, Sweden.ORCID http://orcid.org/0000-0001-9828-9794
Ming-Dong Zhang *Department of Medical Biochemistry and Biophysics, Division of Molecular Neurobiology, Karolinska Institutet, Stockholm, Sweden.ORCID http://orcid.org/0000-0002-6348-1994
Jussi Kupari *Department of Medical Biochemistry and Biophysics, Division of Molecular Neurobiology, Karolinska Institutet, Stockholm, Sweden.
Dongoh KwakDepartment of Medical Biochemistry and Biophysics, Division of Molecular Neurobiology, Karolinska Institutet, Stockholm, Sweden.
Laurence PictonDepartment of Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Bingze XuDepartment of Medical Biochemistry and Biophysics, Division of Immunology, Karolinska Institutet, Stockholm, Sweden.
Leandro Flores do NascimentoDepartment of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience, Linköping University, Linköping, Sweden.
Yizhou HuDepartment of Medical Biochemistry and Biophysics, Division of Molecular Neurobiology, Karolinska Institutet, Stockholm, Sweden.ORCID http://orcid.org/0000-0002-2635-0258
Alejandro GonzalezDepartment of Medical Biochemistry and Biophysics, Division of Molecular Neurobiology, Karolinska Institutet, Stockholm, Sweden.ORCID http://orcid.org/0000-0001-7513-2516
Dmitry UsoskinDepartment of Medical Biochemistry and Biophysics, Division of Molecular Neurobiology, Karolinska Institutet, Stockholm, Sweden.ORCID http://orcid.org/0000-0001-9122-6387
Zhongwei XuDepartment of Medical Biochemistry and Biophysics, Division of Immunology, Karolinska Institutet, Stockholm, Sweden.ORCID http://orcid.org/0000-0001-5178-3437
Marcin SzczotDepartment of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience, Linköping University, Linköping, Sweden.ORCID http://orcid.org/0000-0002-3902-059X
Abdeljabbar El ManiraDepartment of Neuroscience, Karolinska Institutet, Stockholm, Sweden.ORCID http://orcid.org/0000-0001-5920-9384
Rikard HolmdahlDepartment of Medical Biochemistry and Biophysics, Division of Immunology, Karolinska Institutet, Stockholm, Sweden.ORCID http://orcid.org/0000-0002-4969-2576
Patrik ErnforsDepartment of Medical Biochemistry and Biophysics, Division of Molecular Neurobiology, Karolinska Institutet, Stockholm, Sweden. patrik.ernfors@ki.se.ORCID http://orcid.org/0000-0002-1140-3986

Funding

EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council) Descending pain 101053091Knut och Alice Wallenbergs Stiftelse (Knut and Alice Wallenberg Foundation) 2019-0059Knut och Alice Wallenbergs Stiftelse (Knut and Alice Wallenberg Foundation) KAW 2023-0006Knut och Alice Wallenbergs Stiftelse (Knut and Alice Wallenberg Foundation) KAW 2024-0031Vetenskapsrådet (Swedish Research Council) 2019-00761Vetenskapsrådet (Swedish Research Council) 2019-01209
6 · The paper itself

Abstract

Although inflammatory processes in rheumatoid arthritis have been described, mechanisms driving pain are poorly defined. Here, we used a multitude of approaches to uncover the neural basis and causes of inflammatory pain. We show in mice with cartilage autoantibody-induced arthritis that early immune activation and a cytokine storm were mainly driven by vascular cells and monocytes/macrophages in the dorsal root ganglion. However, persistently elevated interferons and receptor activation of the MNK1/MNK2-eIF4E signaling pathway at all disease phases caused sensory-motor dysfunction and pain by inducing hyperexcitability and sensitization of a GFRA3

Indexed as

Arthritis, ExperimentalArthritis, RheumatoidInterferonsNeuronal PlasticityPainSensory Receptor CellsSignal TransductionAnimalsGanglia, SpinalHumansMaleMiceMice, Inbred C57BLInterferons

Identifiers

PMID41807847
PMCPMC13156039

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.