Evidence map›Paper›PMID 41785302›Full record

ArticlePLoS biology2026

The adaptor protein TASL is required for age-related B cell emergence and lupus-like disease development in mice.

Julia C Johnstone, Robert Mitchell, Timothy J Vyse, Alexander J Clarke

Abstract read
In one paragraph

Article in PLoS biology, 2026. 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. The SLC15A4-TASL complex is essential for lupus development in mice.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  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

4 authors.

Julia C JohnstoneKennedy Institute of Rheumatology, University of Oxford, Oxford, United Kingdom.
Robert MitchellKennedy Institute of Rheumatology, University of Oxford, Oxford, United Kingdom.
Timothy J VyseDepartment of Medical and Molecular Genetics, School of Basic and Medical Biosciences, King's College London, London, United Kingdom.
Alexander J ClarkeKennedy Institute of Rheumatology, University of Oxford, Oxford, United Kingdom.ORCID https://orcid.org/0000-0003-2846-7860

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The autoimmune disease systemic lupus erythematosus (SLE) is associated with genetic variants in the X-linked gene CXORF21, which encodes the protein TASL. TASL acts as an adaptor in the IRF5 pathway and is necessary for the phosphorylation of IRF5 in response to TLR7 or TLR9 stimulation. Here, we investigate the role of TASL in the humoral immune response, and in the development of lupus in the B6.MRLlpr murine model of SLE. We find that while TASL is dispensable for their development, it is required for the full activation of B cells via TLR9 stimulation, and consequent interferon signaling and inflammatory cytokine expression. Additionally, TASL is crucial for the emergence of age-associated B cells (ABCs), a B cell population derived from the extrafollicular response that increases with age and is expanded in autoimmune disease, and the production of IgG2c antibodies. We also find that deletion of TASL prevents the onset of autoimmunity in the genetically-determined B6.MRLlpr model of lupus.

Indexed as

AgingB-LymphocytesLupus Erythematosus, SystemicAnimalsAutoimmunityDisease Models, AnimalFemaleImmunity, HumoralInterferon Regulatory FactorsMiceMice, Inbred C57BLMice, KnockoutSignal TransductionToll-Like Receptor 7Toll-Like Receptor 9Interferon Regulatory FactorsIrf5 protein, mouseTlr9 protein, mouseToll-Like Receptor 7Toll-Like Receptor 9

Identifiers

PMID41785302
PMCPMC12974799

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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.