Evidence map›Paper›PMID 37930711›Full record

ArticleJournal of leukocyte biology2024

TLR7 activation of age-associated B cells mediates disease in a mouse model of primary Sjögren's disease.

Achamaporn Punnanitinont, Eileen M Kasperek, Chengsong Zhu, Guan Yu, Jeffrey C Miecznikowski, Jill M Kramer

Open access · hybridAbstract read
In one paragraph

Article in Journal of leukocyte biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.8field-weighted citation impact, top 9% of its field
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

16 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
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  13. Review
  14. Unraveled role of TLR7-mediated interferon signaling activation in COVID-19.Frontiers in cellular and infection microbiology · 2025
    Review
  15. Article
  16. Tlr7 drives sex- and tissue-dependent effects in Sjögren's disease.Frontiers in cell and developmental biology · 2024
    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

6 authors at 3 institutions in 1 country.

Achamaporn PunnanitinontDepartment of Oral Biology, School of Dental Medicine, University at Buffalo, State University of New York, 3435 Main Street, 520 Biomedical Research Building, Buffalo, NY 14214, United States.
Eileen M KasperekDepartment of Oral Biology, School of Dental Medicine, University at Buffalo, State University of New York, 3435 Main Street, 520 Biomedical Research Building, Buffalo, NY 14214, United States.
Chengsong ZhuMicroarray and Immune Phenotyping Core Facility, Department of Immunology, University of Texas Southwestern Medical Center, EB3.216 Biocenter (East Campus), 2330, Inwood Rd., Dallas TX 75235, United States.
Guan YuDepartment of Biostatistics, School of Public Health and Health Professions, University at Buffalo, State University of New York, 3435 Main Street, 705 Kimble Tower, Buffalo, NY 14214, United States.
Jeffrey C MiecznikowskiDepartment of Biostatistics, School of Public Health and Health Professions, University at Buffalo, State University of New York, 3435 Main Street, 705 Kimble Tower, Buffalo, NY 14214, United States.
Jill M KramerDepartment of Oral Biology, School of Dental Medicine, University at Buffalo, State University of New York, 3435 Main Street, 520 Biomedical Research Building, Buffalo, NY 14214, United States.ORCID 0000-0001-9828-8556
University at Buffalo, State University of New York · USThe University of Texas Southwestern Medical Center · USUniversity of Pittsburgh · US

Funding

University of Buffalo Clinical and Translational Science Institute - Supplement SchulyerUL1TR001412 · NCATS · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI MURPHY, TIMOTHY F · 2015 to 2024
$33.8M
Sjögren's International Collaborative Clinical Alliance Next Generation Studies (SICCA-NextGen)U01DE028891 · NIDCR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SHIBOSKI, CAROLINE HELENE · 2020 to 2024
$4.0M
Advanced Training in Oral BiologyT32DE023526 · NIDCR · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI Stefan Hans-Klaus Ruhl · 2013 to 2026
$3.7M
Analysis of MyD88-mediated immune activation in Sjogrens syndrome pathogenesisR01DE029472 · NIDCR · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI Jill Marie Kramer · 2020 to 2026
$2.7M
Individual Predoctoral Scientist FellowshipF30DE014831 · NIDCR · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI KRAMER, JILL MARIE · 2002 to 2005
$139k
Role of TLR7-mediated B cell activation in primary Sjogren’s syndromeF31DE032884 · NIDCR · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI PUNNANITINONT, ACHAMAPORN · 2023 to 2024
$59k
INTERNATIONAL RESEARCH REGISTRY NETWORK FOR SJOGERNS SYNDROME-268032636N01DE032636 · NIDCR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GREENSPAN, JOHN · 2005 to 2006
–
NCATS NIH HHS UL1 TR001412NIDCR NIH HHS F30 DE014831NIDCR NIH HHS F31 DE032884NIDCR NIH HHS N01 DE032636NIDCR NIH HHS R01 DE029472NIDCR NIH HHS T32 DE023526NIDCR NIH HHS U01 DE028891
6 · The paper itself

Abstract

Primary Sjögren's disease (pSD) (also referred to as Sjögren's syndrome) is an autoimmune disease that primarily occurs in women. In addition to exocrine gland dysfunction, pSD patients exhibit B cell hyperactivity. B cell-intrinsic TLR7 activation is integral to the pathogenesis of systemic lupus erythematosus, a disease that shares similarities with pSD. The role of TLR7-mediated B cell activation in pSD, however, remains poorly understood. We hypothesized that age-associated B cells (ABCs) were expanded in pSD and that TLR7-stimulated ABCs exhibited pathogenic features characteristic of disease. Our data revealed that ABC expansion and TLR7 expression were enhanced in a pSD mouse model in a Myd88-dependent manner. Splenocytes from pSD mice showed enhanced sensitivity to TLR7 agonism as compared with those derived from control animals. Sort-purified marginal zone B cells and ABCs from pSD mice showed enhanced inflammatory cytokine secretion and were enriched for antinuclear autoantibodies following TLR7 agonism. Finally, IgG from pSD patient sera showed elevated antinuclear autoantibodies, many of which were secreted preferentially by TLR7-stimulated murine marginal zone B cells and ABCs. These data indicate that pSD B cells are hyperresponsive to TLR7 agonism and that TLR7-activated B cells contribute to pSD through cytokine and autoantibody production. Thus, therapeutics that target TLR7 signaling cascades in B cells may have utility in pSD patients.

Indexed as

Antibodies, AntinuclearSjogren's SyndromeAnimalsAutoantibodiesCytokinesDisease Models, AnimalFemaleHumansMiceToll-Like Receptor 7Antibodies, AntinuclearAutoantibodiesCytokinesTLR7 protein, humanToll-Like Receptor 7ABCAutoantibodiesAutoimmunityNOD.B10RNA binding proteinsT-bet

Identifiers

PMID37930711
PMCPMC10990110
OpenAlexW4388423525

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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 OpenQuestion graph.