Evidence map›Paper›PMID 28067896›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2017

Pathogenic role of endogenous TNF-α in the development of Sjögren's-like sialadenitis and secretory dysfunction in non-obese diabetic mice.

Jing Zhou, Toshihisa Kawai, Qing Yu

Open access · bronzeAbstract read
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

31 citing papers in PubMed, 50 citations in OpenAlex.

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  14. Plasmacytoid dendritic cells promote the pathogenesis of Sjögren's syndrome.Biochimica et biophysica acta. Molecular basis of disease · 2022
    Article
  15. Article
  16. Immunobiology of T Cells in Sjögren's Syndrome.Clinical reviews in allergy & immunology · 2021
    Review
  17. Article
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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 ZhouDepartment of Immunology and Infectious Diseases, The Forsyth Institute, Cambridge, MA, USA.
Toshihisa KawaiDepartment of Immunology and Infectious Diseases, The Forsyth Institute, Cambridge, MA, USA.
Qing YuDepartment of Immunology and Infectious Diseases, The Forsyth Institute, Cambridge, MA, USA.
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
NIDCR NIH HHS R01 DE023838
6 · The paper itself

Abstract

Patients with Sjögren's syndrome (SS), an autoimmune disease primarily affecting exocrine glands, exhibit enhanced TNF-α expression in the saliva and salivary glands. However, the precise in vivo role of TNF-α during the initiation and development of SS is not clearly defined. The present study is undertaken to determine the function of endogenously produced TNF-α in the pathogenesis of SS in non-obese diabetic (NOD) mice, a model of this human disease. Administration of a neutralizing anti-TNF-α antibody to female NOD mice during the stage prior to disease onset significantly improved salivary secretion, indicating a remission of clinical symptoms of SS. TNF-α blockade also decreased the number of leukocyte foci and reduced the number of T cells and B cells in the submandibular glands (SMG). Moreover, TNF-α blockade reduced T-bet protein levels in the SMG, suggesting a decrease in T helper 1 and T cytotoxic 1 cells. These cellular changes induced by TNF-α neutralization were associated with a reduction in T- and B-cell chemoattractants CXCL9 and CXC13. In addition, TNF-α blockade markedly increased the expression level of tight junction protein claudin-1 and water channel protein aquaporin-5, two key factors required for normal salivary secretion, in the SMG. Collectively, these findings indicate that endogenous TNF-α has a pathogenic role in the development of SS in the NOD model of this disease.

Indexed as

AnimalsAntibodies, AntinuclearAntibodies, NeutralizingAquaporin 5B-LymphocytesChemokine CXCL13Chemokine CXCL9Claudin-1Disease Models, AnimalFemaleGene ExpressionHumansMice, Inbred NODMicroscopy, FluorescenceReverse Transcriptase Polymerase Chain ReactionSalivaAntibodies, AntinuclearAntibodies, NeutralizingAquaporin 5Chemokine CXCL13Chemokine CXCL9Claudin-1Tumor Necrosis Factor-alpha

Identifiers

PMID28067896
PMCPMC5376226
OpenAlexW2568991061

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.