Evidence map›Paper›PMID 40743682›Full record

ArticleJournal of autoimmunity2025

Tlr9 expression protects against Tlr7-dependent exocrine gland and systemic disease manifestations in primary Sjögren's disease in a sex-biased manner.

Sheta Biswas, Eileen M Kasperek, Chengsong Zhu, Jeffrey C Miecznikowski, Jason Osinski, Rose-Anne Romano, Jill M Kramer

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of autoimmunity, 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.

Sheta BiswasDepartment of Oral Biology, School of Dental Medicine, The University at Buffalo, State University of New York, Buffalo, NY, USA; Department of Biochemistry and Molecular Biology, Noakhali Science and Technology University, Noakhali, 3814, Bangladesh. Electronic address: shetabis@buffalo.edu.
Eileen M KasperekDepartment of Oral Biology, School of Dental Medicine, The University at Buffalo, State University of New York, Buffalo, NY, USA. Electronic address: emkasprk@buffalo.edu.
Chengsong ZhuDepartment of Immunology, Microarray & Immune Phenotyping Core Facility, University of Texas Southwestern Medical Center, Dallas, TX, USA. Electronic address: Chengsong.Zhu@UTSouthwestern.edu.
Jeffrey C MiecznikowskiDepartment of Biostatistics, School of Public Health and Health Professions, The University at Buffalo, State University of New York, Buffalo, NY, USA. Electronic address: jcm38@buffalo.edu.
Jason OsinskiDepartment of Oral Biology, School of Dental Medicine, The University at Buffalo, State University of New York, Buffalo, NY, USA. Electronic address: josinski@buffalo.edu.
Rose-Anne RomanoDepartment of Oral Biology, School of Dental Medicine, The University at Buffalo, State University of New York, Buffalo, NY, USA. Electronic address: rromano2@buffalo.edu.
Jill M KramerDepartment of Oral Biology, School of Dental Medicine, The University at Buffalo, State University of New York, Buffalo, NY, USA. Electronic address: jkramer@buffalo.edu.

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
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
Spinning disk confocal microscopeS10OD025204 · OD · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI KAY, JASON G · 2019 to 2019
$488k
NCATS NIH HHS UL1 TR001412NIDCR NIH HHS R01 DE029472NIH HHS S10 OD025204
6 · The paper itself

Abstract

Primary Sjogren's disease (pSD) is a systemic autoimmune disease. Currently, the causes of pSD remain unknown, and no curative therapies are available. Our prior studies showed Tlr7 activation was an important driver of pSD in females. Since Tlr7 is regulated by Tlr9, we hypothesized that ablation of Tlr9 would exacerbate disease in a Tlr7-dependent manner. Towards this end, we generated pSD mice that lacked systemic expression of either Tlr9 (NOD.B10

Indexed as

Membrane GlycoproteinsSjogren's SyndromeToll-Like Receptor 7Toll-Like Receptor 9AnimalsAutoantibodiesB-LymphocytesDisease Models, AnimalFemaleHumansMaleMiceMice, Inbred NODMice, KnockoutSex FactorsAutoantibodiesMembrane GlycoproteinsTlr7 protein, mouseTlr9 protein, mouseToll-Like Receptor 7Toll-Like Receptor 9AutoantibodyAutoimmunityB cellMyD88Salivary glandSialadenitis

Identifiers

PMID40743682
PMCPMC12372938

What OpenQuestion holds

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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.