Evidence map›Paper›PMID 30248522›Full record

ReviewCurrent opinion in immunology2018

Extracellular matrix and the maintenance and loss of peripheral immune tolerance in autoimmune insulitis.

Carlos O Medina, Nadine Nagy, Paul L Bollyky

Abstract readReview
In one paragraph

Review in Current opinion in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
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  5. Article
  6. Article
  7. Review
  8. Article
  9. Extracellular matrix protein N-glycosylation mediates immune self-tolerance inProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  10. Article
  11. 4-Methylumbelliferone suppresses hyaluronan and adipogenesis in primary cultured orbital fibroblasts from Graves' orbitopathy.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2020
    Article
  12. Advances in research on the interaction between inflammation and cancer.The Journal of international medical research · 2020
    Review
  13. Article
  14. Article
  15. 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

3 authors at 1 institution in 1 country.

Carlos O MedinaDivision of Infectious Diseases and Geographic Medicine, Dept. of Medicine, Stanford University School of Medicine, Beckman Center, 279 Campus Drive, Stanford, CA, 94305, United States.
Nadine NagyDivision of Infectious Diseases and Geographic Medicine, Dept. of Medicine, Stanford University School of Medicine, Beckman Center, 279 Campus Drive, Stanford, CA, 94305, United States.
Paul L BollykyDivision of Infectious Diseases and Geographic Medicine, Dept. of Medicine, Stanford University School of Medicine, Beckman Center, 279 Campus Drive, Stanford, CA, 94305, United States. Electronic address: pbollyky@stanford.edu.
Stanford University · US

Funding

MOLECULAR &CELLULAR IMMUNOBIOLOGYT32AI007290 · NIAID · STANFORD UNIVERSITY · PI Sean Curtis Bendall, Olivia M Martinez · 1985 to 2026
$27.0M
Stanford Islet Research CoreP30DK116074 · NIDDK · STANFORD UNIVERSITY · PI Seung K Kim · 2017 to 2026
$19.5M
Tissue Cytokine Sequestration and Immune Regulation in AutoimmunityU01AI101984 · NIAID · STANFORD UNIVERSITY · PI BOLLYKY, PAUL L · 2012 to 2021
$5.0M
Lymph Node Extracellular Matrix in Antigen Presentation and Immune RegulationR01DK096087 · NIDDK · STANFORD UNIVERSITY · PI BOLLYKY, PAUL L · 2012 to 2021
$3.4M
ECM Costimulation of Immunoregulatory Pathways in Airway InflammationR01HL113294 · NHLBI · STANFORD UNIVERSITY · PI BOLLYKY, PAUL L · 2012 to 2016
$2.0M
The Development of 4-methylumbelliferone Pro-drugs to Prevent Autoimmune DiabetesR01DK114174 · NIDDK · STANFORD UNIVERSITY · PI BOLLYKY, PAUL L · 2018 to 2020
$1.3M
NHLBI NIH HHS R01 HL113294NIAID NIH HHS U01 AI101984NIDDK NIH HHS P30 DK116074NIDDK NIH HHS R01 DK096087NIDDK NIH HHS R01 DK114174
6 · The paper itself

Abstract

There is a growing appreciation that the extracellular matrix (ECM) contributes to both the maintenance of immune tolerance in healthy tissues and to its loss at sites of autoimmunity. Here, we review recent literature on the role of ECM and particularly the glycosaminoglycans hyaluronan and heparan sulfate in the development of autoimmune, type 1 diabetes (T1D). Data from transplant models suggest that healthy islets are embedded within an intact ECM that supports beta-cell homeostasis and provides physical and immunoregulatory barriers against immune infiltration. However, studies of human insulitis as well as the non-obese diabetic (NOD) and DORmO mouse models of T1D indicate that autoimmune insulitis is associated with the degradation of basement membrane structures, the catabolism of the islet interstitium, and the accumulation of a hyaluronan-rich, pro-inflammatory ECM. Moreover, in these models of autoimmune diabetes, either the pharmacologic inhibition of heparan sulfate catabolism, the reduction of hyaluronan synthesis, or the targeting of the pathways that sense these ECM changes can all prevent beta-cell destruction. Together these data support an emerging paradigm that in healthy islets the local ECM contributes to both immune tolerance and beta-cell homeostasis while in chronic inflammation the islet ECM is permissive to immune infiltration and beta-cell destruction. Therapies that support ECM-mediated 'barrier tolerance' may have potential as adjunctive agents in combination regimens designed to prevent or treat autoimmunity.

Indexed as

AnimalsDiabetes Mellitus, Type 1Extracellular MatrixHumansIslets of LangerhansPeripheral Tolerance

Identifiers

PMID30248522
PMCPMC6286219
OpenAlexW2893389318

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.