Evidence map›Paper›PMID 21926271›Full record

ArticleDiabetes2011

Loss of intra-islet CD20 expression may complicate efficacy of B-cell-directed type 1 diabetes therapies.

David V Serreze, Harold D Chapman, Marijke Niens, Robert Dunn, Marilyn R Kehry, John P Driver, Michael Haller, Clive Wasserfall, Mark A Atkinson

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

49 citing papers in PubMed, 74 citations in OpenAlex.

  1. Review
  2. Review
  3. Advancing Animal Models of Human Type 1 Diabetes.Cold Spring Harbor perspectives in medicine · 2024
    Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. T Cells from NOD-Journal of immunology (Baltimore, Md. : 1950) · 2020
    Article
  15. Review
  16. Article
  17. Article
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  19. Review
  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

9 authors at 3 institutions in 1 country.

David V SerrezeThe Jackson Laboratory, Bar Harbor, Maine, USA. dave.serreze@jax.org
Harold D Chapman
Marijke Niens
Robert Dunn
Marilyn R Kehry
John P Driver
Michael Haller
Clive Wasserfall
Mark A Atkinson
Jackson Laboratory · USUniversity of Florida · USBiogen (United States) · US

Funding

Shared Resource ManagementP30CA034196 · NCI · JACKSON LABORATORY · PI William Carl Skarnes · 1985 to 2026
$61.9M
Diabetogenic Role of MHC Class I Alleles in NOD MiceR01DK046266 · NIDDK · JACKSON LABORATORY · PI SERREZE, DAVID V · 2000 to 2018
$7.2M
ANTIGEN PRESENTING CELL DEFECTS IN AUTOIMMUNE DIABETESR01DK051090 · NIDDK · JACKSON LABORATORY · PI SERREZE, DAVID V · 1996 to 2009
$3.0M
DIABETOGENIC ROLE OF H-2G7 CLASS I ALLELES IN NOD MICER29DK046266 · NIDDK · JACKSON LABORATORY · PI SERREZE, DAVID V. · 1993 to 1998
–
NCI NIH HHS CA-34196NCI NIH HHS P30 CA034196NIDDK NIH HHS DK-46266NIDDK NIH HHS DK-51090NIDDK NIH HHS R01 DK046266NIDDK NIH HHS R01 DK051090NIDDK NIH HHS R29 DK046266
6 · The paper itself

Abstract

objectiveConsistent with studies in NOD mice, early clinical trials addressing whether depletion of B cells by the Rituximab CD20-specific antibody provides an effective means for type 1 diabetes reversal have produced promising results. However, to improve therapeutic efficacy, additional B-cell-depleting agents, as well as attempts seeking diabetes prevention, are being considered. RESEARCH DESIGN AND

methodsAutoantibodies, including those against insulin (IAAs), are used to identify at-risk subjects for inclusion in diabetes prevention trials. Therefore, we tested the ability of anti-CD20 to prevent diabetes in NOD mice when administered either before or after IAA onset.

resultsThe murine CD20-specific 18B12 antibody that like Rituximab, depletes the follicular (FO) but not marginal zone subset of B cells, efficiently inhibited diabetes development in NOD mice in a likely regulatory T-cell-dependent manner only when treatment was initiated before IAA detection. One implication of these results is that the FO subset of B cells preferentially contributes to early diabetes initiation events. However, most important, the inefficient ability of anti-CD20 treatment to exert late-stage diabetes prevention was found to be attributable to downregulation of CD20 expression upon B cell entry into pancreatic islets.

conclusionsThese findings provide important guidance for designing strategies targeting B cells as a potential means of diabetes intervention.

Indexed as

AnimalsAntibodies, Monoclonal, Murine-DerivedAntigens, CD20AutoantibodiesB-LymphocytesDiabetes Mellitus, Type 1Disease ProgressionFemaleHypoglycemic AgentsIslets of LangerhansLymphocyte DepletionMiceMice, Inbred NODMice, SCIDMolecular Targeted TherapyPlasma CellsAntibodies, Monoclonal, Murine-DerivedAntigens, CD20AutoantibodiesHypoglycemic AgentsRituximab

Identifiers

PMID21926271
PMCPMC3198088
OpenAlexW2134310178

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.