Evidence map›Paper›PMID 41235957›Full record

ArticleArthritis & rheumatology (Hoboken, N.J.)2026

Lifelong Evolution of Autoreactive Plasma Cell Numbers, Affinity, and Anatomic Location in Arthritic K/BxN Mice.

Thibault Vanhoucke, Carlos Castrillon, Odile Richard-Le Goff, Angga Perima, Matteo Broketa, Andrew D Griffiths, Patrick England, François Huetz, Pierre Bruhns

Abstract read
In one paragraph

Article in Arthritis & rheumatology (Hoboken, N.J.), 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
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0citing papers in PubMed
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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

9 authors.

Thibault VanhouckeInstitut Pasteur, Université de Paris, Unit of Antibodies in Therapy and Pathology, Inserm UMR1222, 75015, Paris, France.
Carlos CastrillonInstitut Pasteur, Université de Paris, Unit of Antibodies in Therapy and Pathology, Inserm UMR1222, 75015, Paris, France.
Odile Richard-Le GoffInstitut Pasteur, Université de Paris, Unit of Antibodies in Therapy and Pathology, Inserm UMR1222, 75015, Paris, France.
Angga PerimaInstitut Pasteur, Université de Paris, Unit of Antibodies in Therapy and Pathology, Inserm UMR1222, 75015, Paris, France.
Matteo BroketaInstitut Pasteur, Université de Paris, Unit of Antibodies in Therapy and Pathology, Inserm UMR1222, 75015, Paris, France.
Andrew D GriffithsLaboratoire de Biochimie, ESPCI Paris, PSL Research University, CNRS UMR8231 Chimie Biologie Innovation, Paris, France.
Patrick EnglandInstitut Pasteur, Université Paris Cité, CNRS UMR3528, Plateforme de Biophysique Moléculaire, Paris, 75015, France.
François HuetzInstitut Pasteur, Université de Paris, Unit of Antibodies in Therapy and Pathology, Inserm UMR1222, 75015, Paris, France.
Pierre BruhnsInstitut Pasteur, Université de Paris, Unit of Antibodies in Therapy and Pathology, Inserm UMR1222, 75015, Paris, France.ORCID 0000-0002-4709-8936

Funding

Agence Nationale de la Recherche ANR-22-PEBI-0009 PEPR ACCREDIACAPNET (comité ad hoc de pilotage nationale des essais thérapeutiques et autres recherches) MEMO-BREAKCAPNET (comité ad hoc de pilotage nationale des essais thérapeutiques et autres recherches) MEMO-VOCFondation pour la Recherche Médicale EQU202203014631Institut National de la Santé et de la Recherche MédicaleInstitut Pasteur
6 · The paper itself

Abstract

objectiveThe spontaneous K/BxN mouse model of rheumatoid arthritis has been used extensively to study chronic inflammation, contribution of immune cells, and the primordial role of autoreactive antibodies in disease initiation and severity. Only the ubiquitous enzyme glucose-6-phosphate isomerase (GPI) is the target of IgG autoantibodies secreted by autoreactive plasma cells and plasmablasts in K/BxN mice. Strikingly, the appearance and evolution of these autoreactive IgG-secreting cells (IgG-SC) remain unstudied.

methodsHere, we quantitatively and qualitatively investigated the plasmablast and plasma cell responses by measuring the affinity of their secreted antibody for GPI from single cells in cohorts of K/BxN mice from 3 weeks to 87 weeks old.

resultsAnalysis of more than 36,000 individual IgG-SC from spleen, popliteal lymph nodes, and bone marrow revealed high intercellular variability in affinity for GPI, with variations over three logs, with stable secretion rates over the life of the mice. Autoreactive IgG-SC were detectable at 3 to 4 weeks and reached peak proportions of IgG-SC at 35 weeks before stabilizing. High-affinity anti-GPI IgG-SC appeared only transiently in the 6 to 9 weeks postnatal window, whereas low-affinity IgG-SC represented more than 80% of the response at all time points. Serum anti-GPI IgG antibodies evolved in a similar kinetic manner, peaking in proportion to total IgG and in affinity for GPI at 35 weeks.

conclusionOur results report the dynamic nature of the autoimmune B cell response in the K/BxN model, revealing a transient phase of antibody affinity maturation early in disease that allows high-affinity antibody responses.

Indexed as

Antibody AffinityArthritis, ExperimentalArthritis, RheumatoidAutoantibodiesImmunoglobulin GPlasma CellsAnimalsDisease Models, AnimalGlucose-6-Phosphate IsomeraseLymph NodesMiceSpleenAutoantibodiesGlucose-6-Phosphate IsomeraseImmunoglobulin G

Identifiers

PMID41235957
PMCPMC13054446

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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.