Evidence map›Paper›PMID 32618634›Full record

ReviewCurrent opinion in endocrinology, diabetes, and obesity2020

Endotypes in T1D: B lymphocytes and early onset.

Mia J Smith, John C Cambier, Peter A Gottlieb

Abstract readReview
In one paragraph

Review in Current opinion in endocrinology, diabetes, and obesity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Integrating Omics into Functional Biomarkers of Type 1 Diabetes.Cold Spring Harbor perspectives in medicine · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. Screening and Prevention of Type 1 Diabetes: Where Are We?The Journal of clinical endocrinology and metabolism · 2023
    Review
  9. Review
  10. Advanced Delivery Strategies for Immunotherapy in Type I Diabetes Mellitus.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2023
    Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. 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

3 authors.

Mia J SmithBarbara Davis Center for Diabetes.
John C CambierDepartment of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, Colorado, USA.
Peter A GottliebBarbara Davis Center for Diabetes.

Funding

University of Colorado Anschutz Medical Campus DRCP30DK116073 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI LORI SUSSEL · 2020 to 2026
$10.8M
TrialNet: Diabetes Type 1 PreventionU01DK085509 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI GOTTLIEB, PETER A · 2009 to 2018
$5.8M
Autoimmunity risk alleles compromising B cell anergyR01AI124487 · NIAID · UNIVERSITY OF COLORADO DENVER · PI CAMBIER, JOHN C · 2016 to 2020
$2.5M
Insulin Specific T and B cells in Type 1 DiabetesDP3DK110845 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI CAMBIER, JOHN C, MICHELS, AARON W · 2016 to 2016
$1.7M
B Cells and Type 1 DiabetesR01DK096492 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI CAMBIER, JOHN C · 2012 to 2016
$1.6M
Veterinary Pre-Doctoral Research Scholars ProgramT32OD012201 · OD · COLORADO STATE UNIVERSITY · PI VANDEWOUDE, SUE · 2013 to 2019
$795k
Genetic contribution to loss of B cell anergy during development of type 1 diabetesK01OD028759 · OD · UNIVERSITY OF COLORADO DENVER · PI SMITH, MIA · 2020 to 2024
$567k
Perturbation of B cell anergy in T1DR21AI124488 · NIAID · UNIVERSITY OF COLORADO DENVER · PI CAMBIER, JOHN C · 2016 to 2017
$428k
Genetic risk alleles as drivers of loss of anergic B cells in autoimmunityF30OD021477 · OD · COLORADO STATE UNIVERSITY · PI SMITH, MIA · 2016 to 2017
$79k
NIAID NIH HHS R01 AI124487NIAID NIH HHS R21 AI124488NIDDK NIH HHS DP3 DK110845NIDDK NIH HHS P30 DK116073NIDDK NIH HHS R01 DK096492NIDDK NIH HHS U01 DK085509NIH HHS F30 OD021477NIH HHS K01 OD028759NIH HHS T32 OD012201
6 · The paper itself

Abstract

purpose of reviewAlthough type 1 diabetes (T1D) is characterized by destruction of the pancreatic beta cells by self-reactive T cells, it has become increasingly evident that B cells also play a major role in disease development, likely functioning as antigen-presenting cells. Here we review the biology of islet antigen-reactive B cells and their participation in autoimmune diabetes. RECENT

findingsRelative to late onset, individuals who develop T1D at an early age display increased accumulation of insulin-reactive B cells in islets. This B-cell signature is also associated with rapid progression of disease and responsiveness to B-cell depletion therapy. Also suggestive of B-cell participation in disease is loss of anergy in high-affinity insulin-reactive B cells. Importantly, loss of anergy is seen in patient's healthy first-degree relatives carrying certain T1D risk alleles, suggesting a role early in disease development. SUMMARY: Recent studies indicate that islet-reactive B cells may play a pathogenic role very early in T1D development in young patients, and suggest utility of therapies that target these cells.

Indexed as

Age of OnsetAnimalsB-LymphocytesDiabetes Mellitus, Type 1HumansInsulinInsulin-Secreting CellsIslets of LangerhansTime FactorsT-LymphocytesInsulin

Identifiers

PMID32618634
PMCPMC8049183

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.