Evidence map›Paper›PMID 31214622›Full record

ReviewJournal of immunology research2019

Sjogren's Syndrome and TAM Receptors: A Possible Contribution to Disease Onset.

Richard Witas, Ammon B Peck, Julian L Ambrus, Cuong Q Nguyen

Open access · goldAbstract readReview
In one paragraph

Review in Journal of immunology research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

14 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Efferocytosis in multisystem diseases (Review).Molecular medicine reports · 2022
    Review
  11. Research progress on inflammatory mechanism of primary Sjögren syndrome.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2021
    Review
  12. Article
  13. Article
  14. Review
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 2 institutions in 1 country.

Richard WitasDepartment of Oral Biology, College of Dentistry, University of Florida, Gainesville, FL, USA.ORCID 0000-0001-8694-1925
Ammon B PeckDepartment of Infectious Diseases and Immunology, College of Veterinary Medicine, University of Florida, Gainesville, FL, USA.
Julian L AmbrusDivision of Allergy, Immunology and Rheumatology, SUNY at Buffalo School of Medicine, Buffalo, NY, USA.ORCID 0000-0003-4505-796X
Cuong Q NguyenDepartment of Oral Biology, College of Dentistry, University of Florida, Gainesville, FL, USA.ORCID 0000-0001-5633-4075
University of Florida · USUniversity at Buffalo, State University of New York · US

Funding

Comprehensive Training Program in Oral BiologyT90DE021990 · NIDCR · UNIVERSITY OF FLORIDA · PI Jose A Lemos · 2011 to 2026
$8.2M
Mapping the T cell receptor/antigen complex and identifying the genetic-based treatment in Sjogren’s syndromeR01DE028544 · NIDCR · UNIVERSITY OF FLORIDA · PI NGUYEN, CUONG Q · 2019 to 2023
$2.6M
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 R01 DE028544NIDCR NIH HHS R21 DE023433NIDCR NIH HHS T90 DE021990
6 · The paper itself

Abstract

Sjogren's syndrome (SS) is a chronic, progressive autoimmune disease featuring both organ-specific and systemic manifestations, the most frequent being dry mouth and dry eyes resulting from lymphocytic infiltration into the salivary and lacrimal glands. Like the related autoimmune disease systemic lupus erythematosus (SLE), SS patients and mouse models display accumulation of apoptotic cells and a Type I interferon (IFN) signature. Receptor tyrosine kinases (RTKs) of the Tyro3, Axl, and Mer (TAM) family are present on the surface of macrophages and dendritic cells and participate in phagocytosis of apoptotic cells (efferocytosis) and inhibition of Type I IFN signaling. This review examines the relationship between TAM receptor dysfunction and SS and explores the potential contributions of TAM defects on macrophages to SS development.

Indexed as

AnimalsApoptosisAxl Receptor Tyrosine Kinasec-Mer Tyrosine KinaseDisease Models, AnimalDisease SusceptibilityHumansMiceMice, Inbred C57BLMice, Inbred NODMice, TransgenicProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesSignal TransductionSjogren's SyndromeAxl Receptor Tyrosine Kinasec-Mer Tyrosine KinaseMERTK protein, humanProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesTYRO3 protein, human

Identifiers

PMID31214622
PMCPMC6535826
OpenAlexW2944124521

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.