Evidence map›Paper›PMID 41335463›Full record

ArticleRheumatology (Oxford, England)2026

Fcγ-receptor-activation by circulating immune complexes in systemic autoimmune diseases and its reduction by CD19-CAR T cell therapy.

Merle Freitag, Philipp Kolb, Valeria Falcone, Maren Claus, Pauline Schröder, Ivana Andreeva, Lea Rodon, Meike Ewald, Franca Sophie Deicher, Ayla Nadja Stütz and 7 more

Abstract read
In one paragraph

Article in Rheumatology (Oxford, England), 2026. 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. 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

17 authors.

Merle FreitagDepartment of Hematology, Oncology and Rheumatology, Internal Medicine V, University Hospital Heidelberg, Heidelberg, Germany.
Philipp KolbInstitute of Virology, University Medical Center, Freiburg, Germany.ORCID 0000-0001-7935-217X
Valeria FalconeInstitute of Virology, University Medical Center, Freiburg, Germany.
Maren ClausLeibniz Research Center for Working Environment and Human Factors at TU Dortmund (IfADo), Dortmund, Germany.
Pauline SchröderDepartment of Hematology, Oncology and Rheumatology, Internal Medicine V, University Hospital Heidelberg, Heidelberg, Germany.
Ivana AndreevaDepartment of Hematology, Oncology and Rheumatology, Internal Medicine V, University Hospital Heidelberg, Heidelberg, Germany.
Lea RodonDepartment of Hematology, Oncology and Rheumatology, Internal Medicine V, University Hospital Heidelberg, Heidelberg, Germany.
Meike EwaldDepartment of Hematology, Oncology and Rheumatology, Internal Medicine V, University Hospital Heidelberg, Heidelberg, Germany.
Franca Sophie DeicherDepartment of Hematology, Oncology and Rheumatology, Internal Medicine V, University Hospital Heidelberg, Heidelberg, Germany.
Ayla Nadja StützDepartment of Rheumatology, University Hospital Düsseldorf, Medical Faculty of Heinrich-Heine University, Düsseldorf, Germany.
Jörg H W DistlerDepartment of Rheumatology, University Hospital Düsseldorf, Medical Faculty of Heinrich-Heine University, Düsseldorf, Germany.
Norbert BlankDepartment of Hematology, Oncology and Rheumatology, Internal Medicine V, University Hospital Heidelberg, Heidelberg, Germany.ORCID 0000-0002-9419-1690
Ricardo Grieshaber-BouyerDepartment of Internal Medicine 3, Rheumatology and Clinical Immunology, Friedrich-Alexander-University (FAU) Erlangen-Nürnberg and Universitätsklinikum Erlangen, Erlangen, Germany.
Luis E MuñozDepartment of Internal Medicine 3, Rheumatology and Clinical Immunology, Friedrich-Alexander-University (FAU) Erlangen-Nürnberg and Universitätsklinikum Erlangen, Erlangen, Germany.
Hanns-Martin LorenzDepartment of Hematology, Oncology and Rheumatology, Internal Medicine V, University Hospital Heidelberg, Heidelberg, Germany.
Georg SchettDepartment of Internal Medicine 3, Rheumatology and Clinical Immunology, Friedrich-Alexander-University (FAU) Erlangen-Nürnberg and Universitätsklinikum Erlangen, Erlangen, Germany.
Wolfgang MerktDepartment of Hematology, Oncology and Rheumatology, Internal Medicine V, University Hospital Heidelberg, Heidelberg, Germany.ORCID 0000-0002-3108-154X

Funding

Deutsche Gesellschaft für Innere Medizin KO6815/1-11
6 · The paper itself

Abstract

objectivesThe role of autoantibody-producing B cells in connective tissue diseases (CTD) has recently been highlighted by the successful treatment with CD19-targeting CAR T cells. Detrimental effects of autoantibodies are linked to the formation of deposited IgG complexes and the activation of immune cells via Fcγ receptors (FcγRs). The role of circulating immune complexes (cICs) as a link between adaptive and innate immunity has remained understudied. Clinical testing of cICs has been hindered by the lack of reliable detection methods. The aim of this study was to determine the potential of IgG-containing cICs to activate FcγRs (their bioactivity) using a new detection method.

methodsA reporter cell platform was used to assess the presence and bioactivity of cICs in IgG-autoantibody-positive CTD patients (cross-section analysis) and in patients treated with CD19-CAR T cells (longitudinal analysis).

resultsThe bioactivity of cICs in the cohort of patients with CTDs was significantly higher compared with healthy controls and patients with IgG-autoantibody-negative systemic inflammatory disease (psoriatic arthritis). Analyses of individual diseases revealed the presence of cICs in the sera of all CTDs, including systemic sclerosis (SSc) and primary Sjögren's syndrome, although there was significant heterogeneity among individuals. Within SSc, patients positive for anti-topoisomerase-I (Scl70) autoantibodies, diffuse cutaneous and lung involvement had significantly enhanced cIC bioactivity. Finally, the bioactivity of cICs was significantly reduced in CTD patients after CD19-CAR T cell therapy.

conclusionsOur study reveals the presence of FcγR-engaging cICs in CTDs and demonstrates that the bioactivity of cICs is correlated with clinical phenotypes and treatment outcomes.

Indexed as

Antigen-Antibody ComplexAutoimmune DiseasesConnective Tissue DiseasesImmunotherapy, AdoptiveReceptors, IgGAdultAgedAntigens, CD19AutoantibodiesFemaleHumansImmunoglobulin GMaleMiddle AgedAntigen-Antibody ComplexAntigens, CD19AutoantibodiesImmunoglobulin GReceptors, IgGautoantibodiescirculating immune complexesconnective tissue diseasesFcγ-receptorsinterstitial lung diseaseprimary Sjögren’s syndromesystemic sclerosis

Identifiers

PMID41335463
PMCPMC13017110

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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.