Evidence map›Paper›PMID 40037793›Full record

ArticleJournal of the peripheral nervous system : JPNS2025

Cytokine Signature Unveils Subgroups of Patients With Immune-Mediated Sensory Neuronopathies.

Christian P Moritz, Yannick Tholance, Coralie Borowczyk, Fabienne Jospin, Stéphane Paul, Jean-Christophe Antoine, Jean-Philippe Camdessanché

Abstract read
In one paragraph

Article in Journal of the peripheral nervous system : JPNS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

7 authors.

Christian P MoritzSynaptopathies and Autoantibodies (SynatAc) Team, Institute MeLis NeuroMyoGène, INSERM U1314/CNRS UMR 5284, Université Claude Bernard Lyon 1, Lyon, France.ORCID 0000-0002-9294-2323
Yannick TholanceSynaptopathies and Autoantibodies (SynatAc) Team, Institute MeLis NeuroMyoGène, INSERM U1314/CNRS UMR 5284, Université Claude Bernard Lyon 1, Lyon, France.
Coralie BorowczykSynaptopathies and Autoantibodies (SynatAc) Team, Institute MeLis NeuroMyoGène, INSERM U1314/CNRS UMR 5284, Université Claude Bernard Lyon 1, Lyon, France.
Fabienne JospinCIRI - Centre International de Recherche en Infectiologie, Team GIMAP, Univ Lyon, Université Claude Bernard Lyon 1, Inserm, U1111, CNRS, UMR530, CIC 1408 Vaccinology, Saint-Etienne, France.
Stéphane PaulCIRI - Centre International de Recherche en Infectiologie, Team GIMAP, Univ Lyon, Université Claude Bernard Lyon 1, Inserm, U1111, CNRS, UMR530, CIC 1408 Vaccinology, Saint-Etienne, France.
Jean-Christophe AntoineSynaptopathies and Autoantibodies (SynatAc) Team, Institute MeLis NeuroMyoGène, INSERM U1314/CNRS UMR 5284, Université Claude Bernard Lyon 1, Lyon, France.
Jean-Philippe CamdessanchéSynaptopathies and Autoantibodies (SynatAc) Team, Institute MeLis NeuroMyoGène, INSERM U1314/CNRS UMR 5284, Université Claude Bernard Lyon 1, Lyon, France.

Funding

Agence Nationale de la Recherche ANR-18-RHUS-0012Association Française contre les Myopathies AFM-MyoNeurALP2Centre Hospitalier Universitaire of Saint-ÉtienneFondation GroupamaFondation pour la Recherche Médicale DQ20170336751
6 · The paper itself

Abstract

BACKGROUND AND

aimsImmune-mediated sensory neuronopathies (SNN) can occur alongside autoimmune disorders (e.g., Sjögren syndrome), involve autoantibodies (such as anti-FGFR3 or anti-AGO antibodies), or present in isolation. The underlying mechanisms remain unclear. This study aimed to investigate the role of proinflammatory cytokines in these conditions.

methodsBlood levels of IL-1β, IL-6, IL-17, TNF-α, INF α-2, and INF-γ were measured using a Bioplex T200 platform and the Bio-Plex Pro Reagent Kit III in 113 patients with SNN between 2.4 and 464.4 months after symptom onset, categorized based on disease course (acute, subacute, chronic). Eighteen patients had anti-AGO antibodies, 48 had anti-FGFR3 antibodies, and 14 had an autoimmune disease without detectable anti-AGO or FGFR3 antibodies. Disease extent was measured by the SNN score, while the disease severity was evaluated using the modified Rankin score. Immunoreactivity against IL-6 and INF-γ was measured via ELISA.

resultsMulticomponent analysis utilizing cytokines levels identified four distinct patient subgroups characterized by differences in age at onset and SNN score. No significant differences were observed among the subgroups regarding disease course and severity, presence of anti-AGO or anti-FGFR3 antibodies, or association with an autoimmune disease. A small subgroup of three younger patients exhibited the highest levels of TNF-α, IL-6, and IL-1β. Another subgroup of seven patients displayed elevated INF α-2 levels and tended towards highest SNN scores. The largest group (95 subjects) comprised older individuals with relatively lower cytokine levels and decreased anti-IL-6 immunoreactivity.

interpretationThese cytokine profiles suggest diverse underlying mechanisms within immune-mediated SNN. Further investigation is warranted to determine whether certain profiles, particularly those involving young patients with elevated proinflammatory cytokines, might benefit from targeted treatments.

Indexed as

Autoimmune Diseases of the Nervous SystemCytokinesAdultAgedAutoantibodiesFemaleHumansMaleMiddle AgedReceptor, Fibroblast Growth Factor, Type 3Young AdultAutoantibodiesCytokinesFGFR3 protein, humanReceptor, Fibroblast Growth Factor, Type 3anti‐cytokine antibodiescytokinescytokine signatureinterleukinssensory neuronopathy

Identifiers

PMID40037793
PMCPMC11879705

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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.