Evidence map›Paper›PMID 34780913›Full record

ArticleBiochimica et biophysica acta. Molecular basis of disease2022

Plasmacytoid dendritic cells promote the pathogenesis of Sjögren's syndrome.

Jing Zhou, Xiaofeng Zhang, Qing Yu

Open access · greenAbstract read
In one paragraph

Article in Biochimica et biophysica acta. Molecular basis of disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
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  10. The Role of Deregulated MicroRNAs in Immune Cells of Sjögren's Disease.International journal of general medicine · 2025
    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

3 authors at 1 institution in 1 country.

Jing ZhouThe Forsyth Institute, 245 First Street, Cambridge, MA 02142, USA; Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, 188 Longwood Avenue, Boston, MA 02115, USA. Electronic address: jzhou@forsyth.org.
Xiaofeng ZhangThe Forsyth Institute, 245 First Street, Cambridge, MA 02142, USA; Department of Cancer Biology, Dana-Farber Cancer Institute, 450 Brookline Ave, Boston, MA 02215, USA; Department of Medicine, Harvard Medical School, 450 Brookline Ave, Boston, MA 02215, USA.
Qing YuThe Forsyth Institute, 245 First Street, Cambridge, MA 02142, USA; Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, 188 Longwood Avenue, Boston, MA 02115, USA. Electronic address: qyu@forsyth.org.
Harvard University · US

Funding

Regulation and Function of Interleukin-7 in Primary Sjogrens SyndromeR01DE023838 · NIDCR · ADA FORSYTH INSTITUTE, INC. · PI YU, QING · 2014 to 2018
$2.4M
Intermittent fasting restores salivary gland function in Sjögren’s syndromeR01DE030646 · NIDCR · ADA FORSYTH INSTITUTE, INC. · PI ZHOU, JING · 2021 to 2025
$2.3M
Mechanisms and Therapeutic Modulation of T Cell Autoimmune Responses in Sjogren's SyndromeR56DE023838 · NIDCR · ADA FORSYTH INSTITUTE, INC. · PI CHA, SEUNGHEE, YU, QING · 2020 to 2020
$532k
The Role of Plasmacytoid Dentdritic Cells in the Pathogenesis of Sjogren's SyndromeR03DE028033 · NIDCR · ADA FORSYTH INSTITUTE, INC. · PI ZHOU, JING · 2019 to 2020
$398k
Role of Interleukin-22 in the Salivary Gland Disorder in Autoimmune Sjögren's SyndromeR03AI142273 · NIAID · ADA FORSYTH INSTITUTE, INC. · PI YU, QING · 2019 to 2020
$199k
NIAID NIH HHS R03 AI142273NIDCR NIH HHS R01 DE023838NIDCR NIH HHS R01 DE030646NIDCR NIH HHS R03 DE028033NIDCR NIH HHS R56 DE023838
6 · The paper itself

Abstract

Plasmacytoid dendritic cells (pDCs) produce type I interferons (IFNs) and promote pathogenesis of multiple autoimmune diseases. Autoimmune Sjögren's syndrome (SS) primarily affects salivary and lacrimal glands, causing their inflammation, destruction and dysfunction. pDCs and type I IFN activity are elevated in salivary glands of SS patients, and this study seeks to elucidate the in vivo actions of pDCs in SS pathogenesis using the non-obese diabetic (NOD) mouse model. We confirmed the type I IFN-dependency of SS development in female NOD mice and elevation of pDC-type I IFN in their submandibular glands (SMGs). We administered a pDC-depleting anti-BST2/CD317 antibody to female NOD mice from 4 to 7 weeks of age at the early stage of SS, and assessed SS pathologies at age 10 weeks, the time of disease onset. Depletion of pDCs impeded the development of SMG inflammation and secretory dysfunction. It drastically reduced the amount of type I IFN mRNA and the number of total leukocytes, and T- and B lymphocytes in SMGs. Gene expression analyses showed that pDC depletion markedly diminished SMG expression of IL-7, BAFF, TNF-α, IFN-γ, CXCL9, CXCL11, CD40, CD40L, Lt-α, Lt-β and NOS2. Hence, pDCs critically contribute to the development and onset of SS-like salivary gland exocrinopathy.

Indexed as

AnimalsDendritic CellsFemaleInflammationMiceMice, Inbred BALB CMice, Inbred NODSalivary GlandsSjogren's SyndromeSubmandibular GlandAutoimmune inflammationHyposalivationInnate immune cellsSalivary glandSialadenitisType I interferons

Identifiers

PMID34780913
PMCPMC8714705
OpenAlexW3213262468

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.