Evidence map›Paper›PMID 26453623›Full record

ArticleBiology open2015

Sexual dimorphism in an animal model of Sjögren's syndrome: a potential role for Th17 cells.

Alexandria Voigt, Lida Esfandiary, Cuong Q Nguyen

Open access · goldAbstract read
In one paragraph

Article in Biology open, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Blocking IAgLife sciences · 2022
    Article
  3. Article
  4. Article
  5. Sex-mediated elevation of the specialized pro-resolving lipid mediator levels in a Sjögren's syndrome mouse model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. 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 2 institutions in 1 country.

Alexandria VoigtDepartment of Infectious Diseases and Pathology, College of Veterinary Medicine, University of Florida, 2015 SW 16th Ave, Gainesville, FL 32608, USA.
Lida EsfandiaryDepartment of Infectious Diseases and Pathology, College of Veterinary Medicine, University of Florida, 2015 SW 16th Ave, Gainesville, FL 32608, USA.
Cuong Q NguyenDepartment of Infectious Diseases and Pathology, College of Veterinary Medicine, University of Florida, 2015 SW 16th Ave, Gainesville, FL 32608, USA Center for Orphan Autoimmune Disorders, University of Florida College of Dentistry, 1600 SW Archer Rd, Gainesville, FL 32608, USA Nguyenc@ufl.edu.
University of Florida · USFlorida College · US

Funding

Immuno-pathophysiology of Lymphocytic Foci in Sjogren?s SyndromeR00DE018958 · NIDCR · UNIVERSITY OF FLORIDA · PI NGUYEN, CUONG Q · 2011 to 2013
$717k
Massive analysis of paired TCR chains of TH17 cells in Sjogrens syndrome usingR21DE023433 · NIDCR · UNIVERSITY OF FLORIDA · PI NGUYEN, CUONG Q · 2014 to 2015
$393k
Immune-pathophysiology of lymphocytic foci in Sjogren's syndromeK99DE018958 · NIDCR · UNIVERSITY OF FLORIDA · PI NGUYEN, CUONG Q · 2009 to 2010
$216k
NIDCR NIH HHS K99 DE018958NIDCR NIH HHS R00 DE018958NIDCR NIH HHS R21 DE023433
6 · The paper itself

Abstract

Sjögren's syndrome is a complex autoimmune disease with an array of diverse immunological, genetic and environmental etiologies, making identification of the precise autoimmune mechanism difficult to define. One of the most distinctive aspects of Sjögren's syndrome is the high sexual dimorphism with women affected 10-20 times more than men. It is nearly impossible to study the sexual dimorphic development of Sjögren's syndrome in human patients; therefore it is pertinent to develop an appropriate animal model which resembles human disease. The data indicated that female C57BL/6.NOD-Aec1Aec2 mice developed an earlier onset of sialadenitis with a higher composition of CD3(+) T cells and a 10-fold increase in glandular infiltration of Th17 cells at the onset of clinical disease compared to male mice. Inflammatory Th17 cells of female mice exhibited a stronger proliferation in response to disease-specific antigen than their male counterpart. At the clinical disease stage, altered autoantibody patterns can be detected in females whereas they are seldom observed in male C57BL/6.NOD-Aec1Aec2 mice. Interestingly, male C57BL/6.NOD-Aec1Aec2 mice developed an earlier loss of secretory function, despite the fact that female C57BL/6.NOD-Aec1Aec2 mice exhibited a more rapid secretory loss. This data indicates the strong sexual dimorphism in the SjS-susceptible C57BL/6.NOD-Aec1Aec2 animal model, making it an appropriate animal model to examine human disease.

Indexed as

Animal modelSexual dimorphismSjögren's syndromeTh17 cells

Identifiers

PMID26453623
PMCPMC4728356
OpenAlexW2177140611

What OpenQuestion holds

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LicenceCC BY
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.