Evidence map›Paper›PMID 23817982›Full record

ArticleEuropean journal of immunology2013

Insulinoma-released exosomes activate autoreactive marginal zone-like B cells that expand endogenously in prediabetic NOD mice.

Roman Bashratyan, Huiming Sheng, Danielle Regn, M Jubayer Rahman, Yang D Dai

Open access · bronzeAbstract read
In one paragraph

Article in European journal of immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

32 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Article
  3. How does exosome cause diabetes?Hormones (Athens, Greece) · 2024
    Review
  4. Review
  5. Extracellular vesicles as personalized medicine.Molecular aspects of medicine · 2023
    Review
  6. Article
  7. Extracellular Vesicles in Type 1 Diabetes: A Versatile Tool.Bioengineering (Basel, Switzerland) · 2022
    Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Emerging Roles of Exosomes in T1DM.Frontiers in immunology · 2020
    Review
  17. Article
  18. Article
  19. Article
  20. 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

5 authors at 1 institution in 1 country.

Roman BashratyanDivision of Immune Regulation, Torrey Pines Institute for Molecular Studies, San Diego, CA, USA.
Huiming Sheng
Danielle Regn
M Jubayer Rahman
Yang D Dai
Torrey Pines Institute For Molecular Studies · US

Funding

Exosome-induced innate and antigen-specific immune responses in Type 1 DiabetesR01DK091663 · NIDDK · TORREY PINES INST FOR MOLECULAR STUDIES · PI DAI, YANG D. · 2011 to 2015
$2.0M
NIDDK NIH HHS R01 DK091663NIDDK NIH HHS R01DK091663
6 · The paper itself

Abstract

Exosomes (EXOs) are nano-sized secreted microvesicles that can function as potent endogenous carriers of adjuvant and antigens. To examine a possible role in autoimmunity for EXOs, we studied EXO-induced immune responses in nonobese diabetic (NOD) mice, an autoimmune-prone strain with tissue-specific targeting at insulin-secreting beta cells. EXOs released by insulinoma cells can activate various antigen-presenting cells to secrete several proinflammatory cytokines and chemokines. A subset of B cells responded to EXO stimulation in culture by proliferation, and expressed surface markers representing marginal zone B cells, which was independent of T helper cells. Importantly, splenic B cells from prediabetic NOD mice, but not diabetic-resistant mice, exhibited increased reactivity to EXOs, which was correlated with a high level of serum EXOs. We found that MyD88-mediated innate TLR signals were essential for the B-cell response; transgenic B cells expressing surface immunoglobulin specific for insulin reacted to EXO stimulation, and addition of a calcineurin inhibitor FK506 abrogated the EXO-induced B-cell response, suggesting that both innate and antigen-specific signals may be involved. Thus, EXOs may contribute to the development of autoimmunity and type 1 diabetes in NOD mice, partially via activating autoreactive marginal zone-like B cells.

Indexed as

AnimalsAutoantigensB-LymphocytesCell ProliferationCells, CulturedCytokinesDiabetes Mellitus, ExperimentalDisease SusceptibilityExosomesImmunoglobulinsInflammation MediatorsInsulinLymphocyte ActivationMiceMice, Inbred NODMyeloid Differentiation Factor 88AutoantigensCytokinesImmunoglobulinsInflammation MediatorsInsulinMyeloid Differentiation Factor 88TacrolimusToll-Like ReceptorsAutoimmunityAutoreactive B cellsExosomesNODtype 1 diabetes (T1D)

Identifiers

PMID23817982
PMCPMC3832688
OpenAlexW1863508629

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.