Evidence map›Paper›PMID 27117244›Full record

ReviewCurrent diabetes reviews2017

Beta-cell Specific Autoantibodies: Are they Just an Indicator of Type 1 Diabetes?

Georgia Fousteri, Elio Ippolito, Rizwan Ahmed, Abdel Rahim A Hamad

Open access · greenAbstract readReview
In one paragraph

Review in Current diabetes reviews, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 12% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Gamma-aminobutyric acid for delaying type 1 diabetes mellitus: an update.Annals of pediatric endocrinology & metabolism · 2024
    Article
  7. Anti-Islet Autoantibodies in Type 1 Diabetes.International journal of molecular sciences · 2023
    Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. IL-17 and limits of success.Cellular immunology · 2019
    Review
  17. Article
  18. Article
  19. Article
  20. 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 2 countries.

Georgia FousteriDiabetes Research Institute (DRI), IRCCS San Raffaele Scientific Institute, Milan. Italy.
Elio IppolitoDiabetes Research Institute (DRI), IRCCS San Raffaele Scientific Institute, Milan. Italy.
Rizwan AhmedDepartment of Pathology and of Medicine, Johns Hopkins University School of Medicine, Baltimore. United States.
Abdel Rahim A HamadDepartment of Pathology and of Medicine, Johns Hopkins University School of Medicine, Baltimore. United States.
Istituti di Ricovero e Cura a Carattere Scientifico · ITJohns Hopkins University · US

Funding

Mechanisms of Fas Ligand Control of Insulitis in Autoimmune DiabetesR01AI099027 · NIAID · JOHNS HOPKINS UNIVERSITY · PI HAMAD, ABDEL RAHIM · 2013 to 2017
$2.0M
NIAID NIH HHS R01 AI099027
6 · The paper itself

Abstract

backgroundAutoantibodies (AAbs) against islet autoantigens (AAgs) are used for type 1 diabetes (T1D) diagnosis and prediction. Islet-specific AAbs usually appear early in life and may fluctuate in terms of number and titer sometimes for over 20 years before T1D develops. Whereas their predictive power is high for pediatric subjects with high genetic risk who rapidly progress to multiple AAb positivity, they are less reliable for children with low genetic risk, single AAb positivity and slow disease progression.

objectiveIt is unknown how AAbs develop and whether they are involved in T1D pathogenesis. So far an increase in AAb number seems to only indicate AAg spreading and progression towards clinical T1D. The goal of this review is to shed light on the possible involvement of AAbs in T1D development.

methodWe thoroughly review the current literature and discuss possible mechanisms of AAb development and the roles they may play in disease pathogenesis.

resultsGenetic and environmental factors instigate changes at the molecular and cellular levels that promote AAb development. Although direct involvement of AAbs in T1D is less clear, autoreactive B cells are clearly involved in various immune and autoimmune responses via antigen presentation, immunoregulation and cytokine production.

conclusionOur analysis suggests that understanding the mechanisms that lead to islet-specific AAb development and the diabetogenic processes that autoreactive B cells promote may uncover additional biomarkers and therapeutic targets.

Indexed as

AutoantibodiesDiabetes Mellitus, Type 1HumansImmune ToleranceInsulin-Secreting CellsAutoantibodiesAutoantibodiesbiomarkerdiabetogenesispredictionpreventiontype 1 diabetes

Identifiers

PMID27117244
PMCPMC5266674
OpenAlexW2402624623

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.