Evidence map›Paper›PMID 32376798›Full record

ArticleJCI insight2020

T cell exosome-derived miR-142-3p impairs glandular cell function in Sjögren's syndrome.

Juan Cortes-Troncoso, Shyh-Ing Jang, Paola Perez, Jorge Hidalgo, Tomoko Ikeuchi, Teresa Greenwell-Wild, Blake M Warner, Niki M Moutsopoulos, Ilias Alevizos

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 2 pooled it
3.8field-weighted citation impact, top 6% 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

50 citing papers in PubMed, 2 syntheses or guidelines pooled it, 77 citations in OpenAlex.

  1. Pooled it
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  6. Exosomes as immunomodulators in autoimmune inflammation: implications for primary Sjögren's disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
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  15. Article
  16. Article
  17. [Expression of miR-142 and its relationship with Th17/Treg imbalance in children with autoimmune thyroid disease].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2024
    Article
  18. Review
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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

9 authors at 3 institutions in 2 countries.

Juan Cortes-TroncosoSjögren's Syndrome and Salivary Gland Dysfunction Unit.
Shyh-Ing JangSjögren's Syndrome and Salivary Gland Dysfunction Unit.
Paola PerezAdeno-Associated Virus Biology Section, National Institute of Dental and Craniofacial Research (NIDCR), NIH, Bethesda, Maryland, USA.
Jorge HidalgoProgram of Physiology and Biophysics, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago, Chile.
Tomoko IkeuchiOral Immunity and Inflammation Section, and.
Teresa Greenwell-WildOral Immunity and Inflammation Section, and.
Blake M WarnerSjögren's Syndrome and Salivary Gland Dysfunction Unit.
Niki M MoutsopoulosOral Immunity and Inflammation Section, and.
Ilias AlevizosSjögren's Syndrome and Salivary Gland Dysfunction Unit.
Rome Foundation · USNational Institute of Dental and Craniofacial Research · USUniversity of Chile · CL

Funding

Clinical Investigations of Sjogren's SyndromeZIADE000704 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI WARNER, BLAKE · 2009 to 2025
$22.3M
Imaging CoreZICDE000750 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI DOYLE, ANDREW · 2019 to 2025
$6.9M
NIDCR DIR Clinical TrainingZIEDE000727 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI MAYS, JACQUELINE · 2009 to 2025
$6.8M
Intramural NIH HHS ZIC DE000750
6 · The paper itself

Abstract

Sjögren's syndrome (SS) is a systemic autoimmune disease that mainly affects exocrine salivary and lacrimal glands. Local inflammation in the glands is thought to trigger glandular dysfunction and symptoms of dryness. However, the mechanisms underlying these processes are incompletely understood. Our work suggests T cell exosome-derived miR-142-3p as a pathogenic driver of immunopathology in SS. We first document miR-142-3p expression in the salivary glands of patients with SS, both in epithelial gland cells and within T cells of the inflammatory infiltrate, but not in healthy volunteers. Next, we show that activated T cells secreted exosomes containing miR-142-3p, which transferred into glandular cells. Finally, we uncover a functional role of miR-142-3p-containing exosomes in glandular cell dysfunction. We find that miR-142-3p targets key elements of intracellular Ca2+ signaling and cAMP production - sarco(endo)plasmic reticulum Ca2+ ATPase 2b (SERCA2B), ryanodine receptor 2 (RyR2), and adenylate cyclase 9 (AC9) - leading to restricted cAMP production, altered calcium signaling, and decreased protein production from salivary gland cells. Our work provides evidence for a functional role of the miR-142-3p in SS pathogenesis and promotes the concept that T cell activation may directly impair epithelial cell function through secretion of miRNA-containing exosomes.

Indexed as

Epithelial CellsExosomesSalivary GlandsSjogren's SyndromeT-LymphocytesAdenylyl CyclasesAdultAgedCalcium SignalingCell LineFemaleHumansMaleMicroRNAsMiddle AgedRyanodine Receptor Calcium Release Channeladenylate cyclase 9Adenylyl CyclasesATP2A2 protein, humanMicroRNAsMIRN142 microRNA, humanRyanodine Receptor Calcium Release ChannelRyR2 protein, humanSarcoplasmic Reticulum Calcium-Transporting ATPasesAutoimmune diseasesAutoimmunity

Identifiers

PMID32376798
PMCPMC7253014
OpenAlexW3023024905

What OpenQuestion holds

Textmetadata
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.