Evidence map›Paper›PMID 40098342›Full record

ArticleEuropean journal of immunology2025

JAK Inhibitors and B Cell Function: A Comparative Study of Their Impact on Plasma Cell Differentiation, Cytokine Production, and Naïve B Cell Activation.

Wenqi Huang, Charlotte de Vries, Ravi Kumar Sharma, Kittikorn Wangriatisak, Katerina Chatzidionysiou, Vivianne Malmström, Caroline Grönwall

Abstract readComparative Study
In one paragraph

Article in European journal of immunology, 2025. 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. 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.

Wenqi HuangDivision of Rheumatology, Department of Medicine Solna, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden.
Charlotte de VriesDivision of Rheumatology, Department of Medicine Solna, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden.
Ravi Kumar SharmaDivision of Rheumatology, Department of Medicine Solna, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden.ORCID 0000-0002-2658-0002
Kittikorn WangriatisakDivision of Rheumatology, Department of Medicine Solna, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden.
Katerina ChatzidionysiouDivision of Rheumatology, Department of Medicine Solna, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden.
Vivianne MalmströmDivision of Rheumatology, Department of Medicine Solna, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden.ORCID 0000-0001-9251-8082
Caroline GrönwallDivision of Rheumatology, Department of Medicine Solna, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden.ORCID 0000-0002-9111-5537

Funding

Reumatikerförbundet R-994284Stiftelsen Konung Gustaf V:s 80-årsfond FAI-2023-0956Stockholm regionVetenskapsrådet 2023-02497
6 · The paper itself

Abstract

B cells play a crucial role in autoimmune diseases, as evidenced by autoantibody responses and the effectiveness of B cell-targeted therapies. Janus kinase inhibitors (JAKi), which target downstream signaling of cytokine receptors, are potent rheumatic disease-modifying drugs. However, besides reducing inflammation, JAKi may impact the adaptive immune system. In this study, we examined the effects of JAKi on B-cell function using in vitro cultures and multiparameter flow cytometry. The results show a JAKi-mediated reduction in plasma cell differentiation, primarily by inhibition of memory B-cell stimulation and proliferation. JAKi exposure resulted in stalling R848, IL-2, and IL-21 stimulated B cells in an intermediate activated state with elevated naïve cells displaying increased expression of CXCR5, CD71, CD22, and CD20. In addition, the data demonstrate a moderate JAKi-mediated reduction of B cell TNF and IL-8 cytokine expression following stimulation. Importantly, the efficacy varied greatly between drugs; tofacitinib and upadacitinib (pan JAKi; JAK1i) exhibited the strongest impact, while baricitinib (JAK1/JAK2i) showed donor-dependent variation, and filgotinib (JAK1i) had no effect. All JAKi, except filgotinib, inhibited IL-2 or IL-21-induced STAT3 phosphorylation. Still, filgotinib demonstrated similar inhibition of phospho-STAT5 as other JAKi following IL-21. These findings underscore the therapeutic impact of JAKi through the modulation of B-cell functions.

Indexed as

B-LymphocytesCell DifferentiationCytokinesJanus Kinase InhibitorsLymphocyte ActivationPlasma CellsAzetidinesBenzamidesCell ProliferationCells, CulturedHeterocyclic Compounds, 3-RingHumansImidazolesInterleukin-21InterleukinsPiperidinesAzetidinesbaricitinibBenzamidesCytokinesHeterocyclic Compounds, 3-RingImidazolesInterleukin-21InterleukinsJanus Kinase InhibitorsPiperidinesPurinesPyrazolesPyrimidinesPyrrolesresiquimodSulfonamidestofacitinibupadacitinibbaricitinibB‐lymphocytesfilgotinibJAK inhibitortofacitinibupadacitinib

Identifiers

PMID40098342
PMCPMC11914861

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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.