Evidence map›Paper›PMID 40318561›Full record

ArticleJournal of autoimmunity2025

Machine learning approach to single cell transcriptomic analysis of Sjogren's disease reveals altered activation states of B and T lymphocytes.

Maxwell McDermott, Wenyi Li, Yin-Hu Wang, Allen Y Chen, Rodrigo Lacruz, Bettina Nadorp, Stefan Feske

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 1 paper, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed, 1 pooled it
–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

1 citing paper in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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.

Maxwell McDermottDepartment of Pathology, New York University Grossman School of Medicine, New York, NY, 10016, USA.
Wenyi LiDepartment of Pathology, New York University Grossman School of Medicine, New York, NY, 10016, USA.
Yin-Hu WangDepartment of Pathology, New York University Grossman School of Medicine, New York, NY, 10016, USA.
Allen Y ChenDepartment of Medicine, New York University Grossman School of Medicine, New York, NY, 10016, USA.
Rodrigo LacruzDepartment of Molecular Pathobiology, New York University College of Dentistry, New York, NY, 10010, USA.
Bettina NadorpDepartment of Pathology, New York University Grossman School of Medicine, New York, NY, 10016, USA; Department of Medicine, New York University Grossman School of Medicine, New York, NY, 10016, USA.
Stefan FeskeDepartment of Pathology, New York University Grossman School of Medicine, New York, NY, 10016, USA. Electronic address: stefan.feske@nyulangone.org.

Funding

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
Ca2+ signaling via SOCE in the pathogenesis of Sjögren’s syndromeR01DE027981 · NIDCR · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI FESKE, STEFAN, LACRUZ, RODRIGO S. · 2019 to 2023
$2.7M
INTERNATIONAL RESEARCH REGISTRY NETWORK FOR SJOGERNS SYNDROME-268032636N01DE032636 · NIDCR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GREENSPAN, JOHN · 2005 to 2006
–
NIDCR NIH HHS N01 DE032636NIDCR NIH HHS R01 DE027981NIDCR NIH HHS U01 DE028891
6 · The paper itself

Abstract

Sjogren's Disease (SjD) is an autoimmune disorder characterized by salivary and lacrimal gland dysfunction and immune cell infiltration leading to gland inflammation and destruction. Although SjD is a common disease, its pathogenesis is not fully understood. In this study, we conducted a single-cell transcriptome analysis of peripheral blood mononuclear cells (PBMC) from patients with SjD and symptomatic non-SjD controls to identify cell types and functional changes involved in SjD pathogenesis. All PBMCs populations showed marked differences in gene expression between SjD patients and controls, particularly an increase in interferon (IFN) signaling gene signatures. T and B cells of SjD patients displayed a depletion of ribosomal gene expression and pathways linked to protein translation. SjD patients had increased frequencies of naive B cells, which featured a unique gene expression profile (GEP) distinct from controls and had hallmarks of B cell hyperactivation. Non-negative matrix factorization (NMF) also identified several non-overlapping GEPs in CD4

Indexed as

B-LymphocytesLymphocyte ActivationMachine LearningSingle-Cell AnalysisSjogren's SyndromeT-LymphocytesTranscriptomeAdultAgedFemaleGene Expression ProfilingHumansMaleMiddle AgedAutoimmunityCD4(+) T cellsMachine learningSingle-cell RNA sequencingSjogren's diseaseTh1

Identifiers

PMID40318561
PMCPMC12170166

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.