Evidence map›Paper›PMID 30261673›Full record

ArticleInternational journal of molecular sciences2018

Immune Response Targeting Sjögren's Syndrome Antigen Ro52 Suppresses Tear Production in Female Mice.

Marta Trzeciak, Harini Bagavant, Joanna Papinska, Umesh S Deshmukh

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.1field-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

8 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Antibody deposition on vascular endothelial cells contributes to localized inflammation in salivary glands.Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2022
    Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Mechanisms of Disease in Sjögren Syndrome-New Developments and Directions.International journal of molecular sciences · 2020
    Article
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

4 authors at 1 institution in 1 country.

Marta TrzeciakArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA. Marta-Trzeciak@omrf.org.
Harini BagavantArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA. Harini-Bagavant@omrf.org.
Joanna PapinskaArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA. Joanna-Papinska@omrf.org.
Umesh S DeshmukhArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA. Umesh-Deshmukh@omrf.org.
Oklahoma Medical Research Foundation · US

Funding

Innate immunity and autoantibodies in the pathogenesis of Sjogren's SyndromeR01DE025030 · NIDCR · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI DESHMUKH, UMESH S · 2016 to 2020
$2.2M
National Institutes of Health DE025030; DE025030-01A1S1NIDCR NIH HHS R01 DE025030
6 · The paper itself

Abstract

Autoantibodies reactive against Ro52 are present in 70% of Sjögren's syndrome patients and are associated with higher disease severity. However, their role in causing aqueous deficient dry eye, a major cause for morbidity in Sjögren's syndrome, is unclear. To investigate whether immune responses targeting Ro52 contribute towards the dry eye, male and female NZM2758 mice were immunized with recombinant Ro52. Tear production was measured by the phenol red thread test. Sera were analyzed for anti-Ro52 levels by immunoprecipitation. Lacrimal glands were evaluated for inflammatory foci and IgG deposits. Our results showed that, although all mice generated anti-Ro52 antibodies, only females developed a significant drop in tear production. None of the mice developed severe lacrimal gland inflammation, and female mice with anti-Ro52 showed higher levels of IgG deposits within their glands. Passive transfer of anti-Ro52 sera caused reduced tear production in female mice, but not in males. This study demonstrates for the first time that immune responses initiated by Ro52 induce aqueous dry eye, and this may be driven by anti-Ro52 antibodies. Furthermore, the sexual dimorphism in glandular dysfunction suggests that the lacrimal glands in females are more susceptible to autoantibody-mediated injury.

Indexed as

AnimalsFemaleImmunoglobulin GInflammationLacrimal ApparatusMaleMiceRibonucleoproteinsSex FactorsSjogren's SyndromeSS-A AntigenImmunoglobulin GRibonucleoproteinsSS-A Antigendry eyelacrimal glandRo52sexual dimorphismSjögren’s syndrome

Identifiers

PMID30261673
PMCPMC6213551
OpenAlexW2892434548

What OpenQuestion holds

Textmetadata
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.