Evidence map›Paper›PMID 42440430›Full record

ArticleFrontiers in immunology2026

Interleukin-10 at the crossroads of immunity in TLR7-induced lupus.

Johanna Pauline Williams, Anaïs Amend, Anna-Lena Schäfer, Paola Fernanda Ruiz-Aparicio, Antoine Nicolas Kraemer, Aileen Qian Luo, Laura Riechert, Lara Weber, Baerbel Keller, Rudolf Armin Manz and 2 more

Abstract read
In one paragraph

Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Johanna Pauline WilliamsDepartment of Rheumatology and Clinical Immunology, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Anaïs AmendDepartment of Rheumatology and Clinical Immunology, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Anna-Lena SchäferDepartment of Rheumatology and Clinical Immunology, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Paola Fernanda Ruiz-AparicioDepartment of Rheumatology and Clinical Immunology, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Antoine Nicolas KraemerDepartment of Rheumatology and Clinical Immunology, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Aileen Qian LuoDepartment of Rheumatology and Clinical Immunology, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Laura RiechertDepartment of Rheumatology and Clinical Immunology, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Lara WeberDepartment of Rheumatology and Clinical Immunology, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Baerbel KellerDepartment of Rheumatology and Clinical Immunology, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Rudolf Armin ManzInstitute for Systemic Inflammation, University of Lübeck, Lübeck, Germany.
Reinhard Edmund VollDepartment of Rheumatology and Clinical Immunology, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Nina ChevalierDepartment of Rheumatology and Clinical Immunology, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: Systemic lupus erythematosus (SLE) is a prototypical autoimmune disease characterized by dysregulated innate and adaptive immunity. Soluble mediators like cytokines critically shape immune responses and sustain chronic inflammation. Interleukin-10 (IL-10), typically anti-inflammatory, also exerts pro-inflammatory effects in SLE, for example by promoting B cell differentiation and autoantibody production. Despite growing interest in IL-10 as a biomarker or therapeutic target, its dual roles have been reported inconsistently, likely reflecting differences in disease context, clinical presentation, disease activity, and the local microenvironment, an issue addressed in this work. Methods: To further clarify its role in lupus, we investigated its function in a toll-like receptor 7 (TLR7) agonist-induced murine model. By administering an antagonistic anti-IL-10 receptor (anti-IL-10R) antibody, we investigated its broad Results: IL-10 showed both pro- and anti-inflammatory effects on immune cells; however, overall, it modestly limited disease progression, indicating that, under the given conditions, its regulatory, anti-inflammatory effects may slightly outweigh its pro-inflammatory actions. The most pronounced effects were seen in the CD4 T-cell compartment, where IL-10R blockade increased IL-17, while reducing regulatory T cell (T Conclusion: Collectively, these findings highlight dual role of IL-10 in lupus and suggest how a single cytokine may trigger opposing immune effects via shared signaling pathways. Further research is needed to clarify how a pro-inflammatory context directs IL-10 signaling toward stimulatory or suppressive outcomes, informing new therapeutic strategies for diseases such as SLE.

Indexed as

Interleukin-10Lupus Erythematosus, SystemicMembrane GlycoproteinsToll-Like Receptor 7AnimalsDisease Models, AnimalFemaleMiceReceptors, Interleukin-10Signal TransductionT-Lymphocytes, RegulatoryToll-Like Receptor AgonistsIL10 protein, mouseInterleukin-10Membrane GlycoproteinsReceptors, Interleukin-10Tlr7 protein, mouseToll-Like Receptor 7Toll-Like Receptor AgonistsCD4 T cellsexperimental lupusinterleukin-10 (IL-10)regulatory T cellsSLESTATTLR7

Identifiers

PMID42440430
PMCPMC13333421

What Socratic holds

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LicenceCC BY
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Registered trials

None linked

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 Socratic graph.