Evidence map›Paper›PMID 19568172›Full record

ReviewCurrent opinion in rheumatology2009

Pathogenesis of Sjögren's syndrome.

Nikolay P Nikolov, Gabor G Illei

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in rheumatology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 2 pooled it
6.7field-weighted citation impact, top 3% 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

75 citing papers in PubMed, 2 syntheses or guidelines pooled it, 154 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Article
  6. Article
  7. Sex Differences in the Lacrimal Gland: Implications for Dry Eye Disease.International journal of molecular sciences · 2025
    Review
  8. Review
  9. Article
  10. Article
  11. Exploring Salivary Epithelial Dysfunction in Sjögren's Disease.International journal of molecular sciences · 2024
    Review
  12. Review
  13. The P2X7 Receptor in Autoimmunity.International journal of molecular sciences · 2023
    Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Sjögren's Syndrome and Viral Infections.Rheumatology and therapy · 2021
    Review

15 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 1 country.

Nikolay P NikolovSjögren's Syndrome Clinic, National Institute of Dental and Craniofacial Research (NIDCR), Molecular Physiology and Therapeutics Branch, National Institutes of Health (NIH), Bethesda, Maryland 20892, USA.
Gabor G Illei
National Institute of Dental and Craniofacial Research · USNational Institutes of Health · US

Funding

Clinical Investigations of Sjogren's SyndromeZIADE000704 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI WARNER, BLAKE · 2009 to 2025
$22.3M
Clinical Investigations Of Sjogren's SyndromeZ01DE000704 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI ILLEI, GABOR · 2002 to 2008
$3.0M
Intramural NIH HHS Z01 DE000704Intramural NIH HHS Z99 DE999999
6 · The paper itself

Abstract

purpose of reviewTo summarize recent developments in our understanding of the pathogenesis of Sjögren's syndrome with a focus on the relationship between inflammation and exocrine dysfunction. RECENT

findingsAnimal models demonstrated the complex interactions between immunologic and nonimmunologic mechanisms in Sjögren's syndrome. Activation of the innate immune system can lead to exocrine dysfunction before or without significant inflammation, whereas in other models, salivary gland function is preserved despite intense inflammatory infiltrates. Primary or inflammation-related abnormalities in water channels contribute to the exocrinopathy. Activation of the innate immunity in patients is demonstrated by the upregulation of type-1 interferon-regulated genes (interferon signature) in peripheral blood and salivary glands and abnormal expression of B cell-activating factor and its receptors. Nonimmune mechanisms that may contribute to exocrine dysfunction include local and systemic androgen deficiency and autonomic nervous system dysfunction. Autoantibodies against the muscarinic acetylcholine receptors would provide a link between autoimmunity and exocrine dysfunction, but the data on the presence, frequency and physiologic affect of these antibodies remain controversial. SUMMARY: Recent discoveries from studies in patients with Sjögren's syndrome and animal models suggest a complex interplay between genetic factors, environmental and stochastic events that involve innate and adaptive immunity, hormonal mechanisms and the autonomic nervous system. Some of these findings suggest that exocrine gland dysfunction may precede autoimmunity or represent a process independent from inflammation in the pathogenesis of Sjögren's syndrome.

Indexed as

AnimalsAutoantibodiesAutonomic Nervous SystemB-Cell Activating FactorCausalityDisease Models, AnimalFemaleHumansInterferon-alphaMaleReceptors, MuscarinicSex CharacteristicsSjogren's SyndromeAutoantibodiesB-Cell Activating FactorInterferon-alphaReceptors, MuscarinicTNFSF13B protein, human

Identifiers

PMID19568172
PMCPMC2766246
OpenAlexW1694838020

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.